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RUTGERS / OTHER / OTH 132 / What is meant by Trichomonas vaginalis?

What is meant by Trichomonas vaginalis?

What is meant by Trichomonas vaginalis?

Description


What makes adaptive/acquired immunity what it is?




Where are all of our immune cells?




Where are these macrophages?



April 10 2017 Start of Exam 4 Material Fungal and Protozoal cells are eukaryotic = not a lot of antifungal or antiprotozoal  agents -the infections are really not common -common in immunocompromised Clinically Important Fungi and Protozoa: Chapter 19 Fungi that invade keratinized tissue (upper part of skin) = called dermatophytes => dermatomycosiIf you want to learn more check out What is an animal glucose storage?
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Don't forget about the age old question of sco 1000
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We also discuss several other topics like Describe the characteristics of hollywood.
s Ex: Ringworm (round circle): Tine corporis, t. cruris, and T. capitis T. inguinum: all contagions from unclean environment = nails T. pedis: can get secondary bacterial infection = athlete’s foot -hard to treat, grow very slow, takes a long time for antifungal agent to kill last organism The spores that fungal cells are part of their life cycle = spores are what we come in contact with = once in body = start actively going into vegetative state Blastomycosis: deeper skin lesion caused by blastomycosis dermatitidis. Normal  entry, wound or lung. Caused by spores. -Complication: systemic blastomycosis -opportunistic Fungal Infection: Candidiasis: Candida albicans, part of normal flora,  can cause thrush, vaginitis, infect tissues when taking antibiotics can be susceptible to these infections -number one nosocomial fungal infection Chap. 20: urogenital and sexually transmitted Trichomonas vaginalis = protozoan transmitted sexually causes trichomoniasis -T hominis in intestine and T. tenzx are normal commensals -picked up virulence factors that caused harm to us -eukaryotic, doesn’t involve spores Respiratory Disease: Chapter 21 Fungal: 1.Coccidiomycosis coccidioides immitis -common in soil, fungal spores-southwest = inhale spores = flue like symptoms which is usually self limiting but is infectious -Complication: spread to meninges or bones for those who are  immunocompromised = serious problem 2. Histoplasmosis: Histoplasma capsulatum -soil harbors fungal spores -endemic in central and eastern u.s. soil fungus spores inhaled =  survive in macrophages = travel through body  Complication: pneumonia infection in spleen, liver, lymph nodes 3. Cryptococcosis: Filobasdiella neoformans -common endospore disease where you inhale spores -budding yeast carried by birds = inhaled or by mouth enter body =  respiratory infection -Complication: systemic = brain -problem in AIDS patient 4. Pneumocystis pneumonia: Pneumocystis jiroveci (carinii)  -Complications spread to other organs -problem in AIDS patient, because they were immunocompromised 5. Asperigillosis: Aspergillus funigatus -veg. skin wound -infects lung from inhaling spores -fungus can form hyphae -complications: invasive infection can lead to asphyxiation -problem in AIDS patients -can die from lack of oxygen -difficult to treat with these different forms that fungal cells take on Chapt. 22: Protozoan Gastrointestinal Disease 1. Giardiasis: Giardia intestinalis (lamblia) -vegetative cells make cysts = ingested cysts (water) = small intestine  = trophozoite adhere to bowel wall = diarrhea with dehydration and interrupts  normal absorption  -Giardia cyst not killed by chlorination-can’t absorb anything from normal intestinal tract -have to think of other ways to treat water because chlorination  doesn’t do anything to cysts 2. Amebiasis: amoebic dysentery caused by Entamoeba histolytica -can be acute disease or chronic -enteric infection, lyses tissue -aggressive disease = perforation in bowel -ingest cysts = trophozoites in colon -can invade intestinal mucosa = get into bloodstream -intestinal lining damage can cause fecal material into the body cavity  “peritonitis” -cysts are not killed by normal chlorine concentrations in water 3. Balantidiasis: Balantidium coli, one of only that are “ciliated” -cysts ingested = trophozoite = invade large intestine wall  -can cause “peritonitis” 4. Cryptosporidiosis -kitten and puppy source = cysts = release protozoa = infect intestine  and can migrate to other tissue  -problem for AIDS patient Chapter 23: Systemic Diseases 1.Leishmaniasis: sand fly bite spreads protozoa = blood stream = macrophages  allow multiplication within  Leishmania donovani = most sever infectious agent -can cause extensive damage to immune system and if left untreated  causes death. -problem for soldiers in countries with tropical climate 2.Malaria: endemic in tropical areas -plasmodium infect red blood cells, get infection from mosquito -interesting life cycle  -people with sickle cell trait are protected from protozoan being able to  replicateApril 12  Innate Host Defenses -Innate involves physical barriers, chemicals, cells that can phagocytize,  inflammation, fever and molecules like interferon and complement which are all  non-specific for the pathogen.  -we respond in a very non-specific way -it could be a virus, anything that enters our body = have a whole series of  processes that prevent the infection from getting established Ex skin barriers, mucous body openings that trap substances -have interferons and perforin and they are chemicals released = lysis of  membranes to break open -neutrophils and dendritic cells and macrophages phagocytize a foreign agent -doesn’t matter if it’s streptococcus pyogenes -things from our skin and stomach = acidic = preventing organisms from  taking up residence -fever = to have slightly induce temp. helps us fight an infection = sense that an organism in us = resetting temp. -complement cascade: important to protect against foreign invaders -Adaptive or Acquired Immunity involves antibody producing cells and T cells  which get help from phagocytes and responds specifically to a pathogen. -responds in a specific way -T cells respond directly to pathogens -both these cells respond to antigen in a specific way -if we ever see that pathogen again, have memory Fig. 16-1 Pluripotent stem cell (in bone marrow) -can break it up into 2 lineages -the myeloid stem cells and the lymphoid stem cells -monocytes = macrophages -dendritic, neutrophils, eosinophils, basophils = macrophages -dendritic = look like neuronal dendrites = macrophage -monocytes and dendritic and neutrophil are phagocytic-monocyte and dendritic play a role in adaptive immunity -these are part of our innate immunity -basophils = release histamines = when there’s damage to skin cells = cause blood vessels to dilates = chemo attractant to macrophages -release histamine = inflammatory response = macrophages come -eosinophils take care of those larger parasitic organisms -worm infections -large worm too big for macrophage to internalize -lymphoid stem cells = b lymphocyte = antibody  Also mature into t lymphocytes = attack foreign cells directly and help b cells  make antibodies -also make NK cells = they wander about = look for those foreign cells that  do not look healthy or like our cells -take care of tumor cells before it develops into cancer Table 16-1 Know summary of what they do and the ones we talked about -don’t worry about percentages -neutrophils: first cells that will recognize a pathogen -respond pretty fast  -don’t last very long, little life span -macrophages: very long life span -acquire different names depending on if they are in blood or tissues -monocyte names dependent on tissue Can be fixed in tissues or wandering in blood and lymph system Phagocytes -Dendritic are more in lymph tissue = presenting antigens to b and t cells -neutrophils and macrophages -process 1. Chemotaxis: by Pattern Recognition Receptors for LPS, Peptidoglycan etc  and by Cytokines-attracted by chemicals released called cytokines or chemokines by  cells in response to pathogen = macrophages release things, b and t cells release  cytokines calling macrophages to come -when we damage mast cells in tissues = chemicals released are  histamines = attract macrophages -macrophages and neutrophils are ciliated to infection due to chemical  attraction = they have receptors that recognize repetitive structures on these  pathogens 2. Adherence -microorganisms may have capsule so that it can’t grab onto it =  macrophage can’t see it -takes place because there are receptors that are recognizing this very  repetitive structure of microorganisms 3. Digestion in the phagolysosome -extracellular Killing = eosinophils (release a Major Basic Protein punches holes and  makes fragments of worm and then digested by macrophages and neutrophils) and  Natural Killer Cells Fig. 16-3 -toll receptors sitting on surface of macrophage -one recognizes a virus or LPS or peptidoglycan -toll, receptors on macrophage look similar to one on fruit flies -gets engulfed and then it is in a phagosome (membrane coming from surface of  macrophage) -nothing happens until phagosome connects with lysosomes -lysosomes help break apart bacteria in phagosome = makes oxidative enzymes,  proteases, lipases, eventually a lot of material can be used by macrophage or will  be excreted Where are these macrophages? Where are all of our immune cells? Lymphatic System -involves lymph fluid, lymph vessels, lymph nodes, spleen, thymus, tonsils,  lymphoid nodules like gut-associated lymphatic tissues -with our innate and adaptive defense mechanisms -innate and adaptive defense mechanisms take place in this system Fig. 16-5 this is where those macrophages and those dendritic cells present the  antigen/pathogen to B and T cells-very important because when we need to respond to a very specific way to a pathogen = need an envt. where they can come together and work together -lymph fluid enters in one direction and leaves in one direction (specifically) -antigen presentation takes place in lymph tissue Another type of innate immunity Fig. 16-6 1. Cut allows bacteria to get beneath surface of skin 2. Damaged cells (basophils and mast cells) release histamine and bradykinin (pain  inducer) 3. Capillaries dilate (vasodilation), bringing more blood to the tissue. Skin becomes  reddened and warmer. 4. Capillaries become more permeable, allowing fluids to accumulate and cause  swelling (edema). 5. Blood clotting occurs, and scab forms 6. Bacteria multiply in cut. 7. Phagocytes enter tissue by moving through the walls of blood vessels  (diapedesis). 8. Phagocytic cells are attracted to bacteria and tissue debris (chemotaxis) and  engulf them. 9. Larger blood vessels dilate, further increasing blood supply to tissue and adding  to heat and redness. 10. As dead cells and debris are removed; epithelial cells proliferate and begin to  grow under the scab. 11. Scar tissue (connective tissue) replaces cells that cannot replace themselves. This is the inflammatory response Granuloma = walling off areas of infections that inside the macrophages -tubercles in mycobacterium tuberculosis -Treponema pallidum = gumma = syphilis -part of innate immunity = containing pathogen Fevers: when an organism comes into body = release factors called pyrogens and  pyrogens could be a toxin = their ultimate goal = increate temp. = our bodies  recognize those pyrogens and they’re very nonspecific = could be a chemical  secreted by organism or toxin = this induces our macrophages to excrete chemicals that cause hypothalamus = body temp. rise = exogenous pyrogen -release factors to cause our body temperatures to riseAdvantage: -organisms don’t want to live at high temp -faster reactions, macrophages work a little bit faster Fig. 16-7 Antiviral response -interferon response -virus comes in and takes over -our cell can release a factor called interferon -this cell is dead -interferon is released and goes to other cells = programmed to release antiviral  proteins = to prevent infection from setting up -this gene in our cells are actually protecting the neighborhood by programming  cells to make antiviral proteins -made in response to viruses and bacterial infections -signal cells to come to tumor cells Are used not only an antipathogen, it also is used in clinics to treat cancer -cloned the interferon gene, used in the clinics to treat certain types of cancer -cancers associated with viruses (HPV) -used to treat viral infections -can have nasty side effects -our own bodies make it Another way of innate immunity against viruses Table 16-3  -cancer cells look different from our cells -once interferon is made = calling in the destruction through making antiviral  proetins Fig. 16-8a Series of proteins that all work together = innate immunity Cascade or pathway = because they work together -series of proteins = they get stimulated to work together when they see a  pathogen -the cascade does 3 things-triggers inflammatory response  -help make macrophages attracted to pathogens = opsonization -some factors physically board down to membrane of pathogen = membrane  attack complexes -can be triggered by 2 different pathways: 1. classical pathway: involves antibody antigen  2. alternative pathway: don’t involve antibodies = extra way of trigger this -back up  Fig. 16-8b show me C1 will react with C4 etc. = don’t need ot know -know the critical points (inflammation, opsonization, and membrane attack  complexes that destroy pathogen) -only become active when C1 recognizes an antibody that’s attached to an  antigen -C1 will bind to C4 = proteolytic cleavage =  -C3b reacts with C5 and C5a and b are chemo attractants to macrophages =  are released in response to a pathogen = attract macrophages and neutrophils to  site of infectious agent = inflammatory response -you’re making chemical factors = triggering inflammatory response = to get  rid of pathogen -mast cells releasing histamine, C3 and C5a attracting macrophages -release a factor called C3b -on macrophage, has receptors that recognize C3b = binds to  pathogen nonspecifically = the receptor see that = grabs onto it = receptor on  macrophage will also recognize antibodies -for this organism, if capsulated and antiphagocytic = can decorate it  with C3b and an antibody = now macrophage has recognized organism =  opsonization -last 3 or 4 complement factors= make a hole = causing lysis -people missing complement factors = immunocompromised Fig. 16-9a Complement lesion Fig 16-9b microscopic pic Fig. 16-10 summary of mechanisms are responding NON-SPECIFICALLY  =have all of these things working for us-if this isn’t enough = we have our adaptive immunity On Monday we will talk about monocytes will help b and t cellsApril 17, 2017 Fig. 16-1  Last week: talked about innate immunity, worried about neutrophils, dendritic cells  and monocytes = phagocytic Tonight: concentrate on lymphoid stem cell lineage -B lymphocyte = antibody producing cells -T lymphocytes (wed night) -NK cells = work independently of other cells = put in lineage because the  proteins expressed put them in lymphoid stem cell line = independent, surveilling  for abnormal tumor cells growing out of control -adaptive/acquired immunity = talking about cells and lymphoid stem cell  lineage -dendritic and monocytes are working with these cell lines to present  antigens -cells involved with innate also are involved with antigen presentation to  lymphoid stem cells (B cells and T cells) Fig. 17-1 Innate immunity: what we’re genetically programmed with -don’t have receptors on our cells that dog virus can enter  -genetic factors: whatever our proteins express = determine whether a  bacterial or virus can infect us -our genetics will allow certain pathogens to infect us = other times don’t  have to worry cause pathogen can’t grow in us Acquired/Adaptive Immunity: -either an active (our bodies are doing something = making antibodies) -also have Passive (means we receive ready-made antibodies = don’t  produce them ourselves = coming from another source) =injections or mother’s milk -breaking up active: -making own antibodies  -natural: antibody response due to infection (see pathogen) after a few days = will start actively making antibodies -exposed to pathogen -artificial active making antibodies = receiving a vaccination=ex: heat killed influenza virus or attenuated bacteria =  let immune system respond = something was given to me to make me make those  antibodies but it’s not an active infection = immunization -naturally we get antibodies from our mother (passive acquired) and from  milk -going to happen because that is nature = we don’t do anything to  create that situation -artificially, passively get antibodies =ex: bitten by rabid dog = start giving you injections of antibodies -ex: bitten by rattle snake = have antivenom = grabs snake venom out of circulation -because you receive that antibody from an outside source = had to be injected with the antibodies Table 17-1 Characteristics of Types of Immunity When you’re recovering from an illness, and you make active antibodies = that Is a  lifetime immunity Ex: can only get chicken pox once -depends on what pathogen is as to whether it’ll be lifelong immunity -active immunity is long lasting = protected -when you get antibodies passively = when injected = have a half life of  maybe a few weeks = eventually proteases will break down antibodies and that’s it -need to receive antibodies again when bitten by rabid dog -baby eats antibodies temporarily from mother -rely on memory for long lasting antibody  Fig. 17-2 -can be DNA, RNA, carbohydrate, protein, glycoprotein, can be a lipid -really depends -an antibody recognizes a specific site and usually is the antigenic  determinant site or epitopes = recognizes a specific sequence -can be 8 amino acids and antibody can see the epitope Ex: flagella: series of amino acids  -making an antibody for 8 amino acids -then upstream in that protein we have a different set of amino acids = different antibody with a different amino acid sequence-2 different epitopes on that one protein -an antibody can see as few as 8 amino acids (epitope) -I have antibodies recognizing this protein (2 different antibodies) -an antigen is creating an immune response -you can have proteins, DNA, RNA, many different types of molecules  will elicit an antibody response Fig. 17-2b -ex: making antibodies for E. coli -I have another antibody recognizing something on pilus -another recognizing something on flagella -all of these things are different epitopes -we have antibody recognizing E. coli -what we’d like to call this antibody = polyclonal antibody (many different  antibodies recognizing different epitopes in that solution that they gave you) -monoclonal antibody: antibody only recognizes one of the epitopes  -only specifically recognizes this specific antigen  -ex: ELISA = the antibodies in that ELISA were monoclonal  specific to strep Antigen = to have the nice clean assay Fig. 17-3 Lineage of Lymphoid Stem cells -we have bone marrow supplying our B cells -where B cells mature = stem cell matures in Bone marrow = b cells =  differentiates into antibody producing cells -T cells mature in thymus = once fully mature = have the capability of being  functioning T cell -ultimately the T and B cells like to hang out in lymph tissue especially  in lymph nodes = ultimately mature to an active antibody secreting cell and T cell  when seeing an appropriate antigen -hang out in a dormant state until antigen is present -don’t want immune system going crazy = allergies -can find both in blood, but are waiting in lymph tissue to be presented with antigen When talking about B and T cells = 2 different types of immunity-B cells = antibody producing cells = secrete antibodies once mature =  humoral immunity because the antibodies are basically in the fluid of your body -T cells = made up of 4 different classes = only going to talk about the T  helpers = tonight going to talk about the T helpers = they respond to antigens  directly on cells = not humoral immunity = cell mediated immunity -interact with other cells = that’s how immune response Is being  developed = secreting factors = T helper cells help B cells make antibodies -some T cells directly find the virally infected cells = kill them  -either secreting facts or directly taking care of those aberrant cells Tonight will talk about T helper cells and how they help B cells make their antibodies Always remember that in immunology = there is a lot of communication between  cells = recognizing one other = how does B cell know where to find that antigen =  have different receptors to communicate = can recognize specifically the different  antigens = that’s how B cells know which T helper cells will help =  adaptive/acquired immunity What makes adaptive/acquired immunity what it is? 4 traits  -B and t cells have these traits Table 17-3 -Recognition of self-versus non-self -makes transplants of tissues very impossible = would be from  identical twin = genetically identical -specificity: be able to recognize a particular antigen in a specific way -T cell response? Do I need an eosinophil? -have a response to any pathogen that might enter my body in course  of my lifetime -heterogeneity: have enough antibodies to recognize any particular antigen  -have to have tremendous ability to make antibodies to any foreign  antigen -Memory: sets acquired away from innate immunity -if I see antigen again = will respond much faster = can prevent any  signs or symptoms of disease -innate: no memory, have phagocytes but there is no memory These 4 attributes are part of B cells and T cells, these are part of our adaptive  immune system, just work a little differently, working togetherFig. 17-5 look at the pictures with the colors and the shapes -shapes of antibody molecules = showing you the different antibodies with  the specificities for the different antigens -we have a whole lot of different B cells responding to different antigens =B cells have on outside of surface = antibodies = antibody is what is  reacting to antigen  -but the antibodies on outside of B cells each are recognizing a unique  antigen -this is where the specificity comes in  -B cell may have molecule (antibody) recognizing this specific antigen -pulling out the particular antigen and B cell responding to one another -all different type so B cells in body (heterogeneity) -specificity = one antibody recognizing green antigen = this green triangle is  making this B cell respond = it’s not responding to nay other b cells because  receptor on surface can’t recognize this -have a T helper cell: going to help this B cell expand = multiplies = go from  1 to 2 to 4  -this T cell is secreting lymphokines, proteins = to help B cell expand = clonal expansion -expanding this one B cell type = B cells mature into plasma cells =  the plasma cells are the cells that secrete the antibodies = b cells mature with help  of t cells because they are secreting lymphokines to get the b cells to mature = into plasma cells secreting one particular antibody (monoclonal) to this little green  triangle on surface of pathogen -have green antigen stimulating on B cell = expanding = need T helper cells = know that this B cell needs help because the b cell will put on its surface a  little bit of antigen and t cells has receptor to green antigen = why the correct T  helper cell comes in and corrects the B cell  -with the help of Helper t cells = will make memory cells = large percentage  of B cells make antibodies = always keep a couple = memory = stored and silent  until next time you see green antigen = B memory cells get stimulated = quicker  immune response next time around = no signs or symptoms -takes care of heterogeneity, specific, memory Now we’re going to talk about cells that are deleted Fig. 17-6 Every cell has different proteins on the outside (potential antigen)-anything on outside of cells = have potential to make antibody to = gets deleted  out of repertoire of cells -if we have this particular antigen = but can make antibody to that = can’t let this  cell stay in system = it’ll destroy tissues = will delete them -any of these B cells that can recognize specific proteins on B cells gets  deleted = clonal deletion -during fetal development any b and t cells that can react with proteins on surface  of cells will be deleted = exactly what we want (autoimmune diseases) -this works but not perfect, other reasons why it develops Fig. 17-7 Antibodies are composed of 2 different chains (light and heavy chain) -it’s a duplication, mirror image = 2 heavy and 2 light chains -light chain: a smaller peptide = fewer amino acids = when you add up  weight of amino acids = much less than the large polypeptide that makes up the  heavy chain = just the number of amino acids in this chain -the heavy and light chain are brought together = by disulfide bonds -the sulfide linkage can form these bonds -can have disulfide bonds between each half of the y molecule = wind  up with 2 heave chains and 2 light chains There are carbohydrate chains attached -the antibody can be divided into 2 segments -variable region: light and heavy chain -on this arm is identical to variable region on other side -one y shaped antibody = combine 2 different antigens -about 2/3 of antibody is the constant region = composed of a part of  light chain and large extension of heavy chain -defines the class of the antibody (IGG or IGM, IGA, = 5 classes  of antibodies) -the constant region is the region that complement binds = C1  will bind here, macrophages (opsonization, decorated with antibodies, macrophage  can recognize it even if it has a capsule) recognizes the specific are of the constant  region), IGG is the only class of antibody that can cross the placenta = baby gets  from mother = from interaction taking place on this portion of IGG -variable region is what recognizes antigenHow is that we would have enough DNA to make all of those antibodies = whole cell would be taken up with DNA = where splicing comes in P480 Can splice different types of DNA together -5 classes of constant regions, and then IGG has number of different subtypes -don’t have antibody segments next to one another = splice them together  =generating diversity = antigen specific binding sites with constant regions -with B cells = splicing occurs -have many variable regions splice together with constant region that we need -can generate many different mRNA regions for light chain -ability to splice and bring in the necessary segments with corresponding constant  regions = diversity = minimum amount of DNA needed = where we see splicing  how our bodies generate diversity -problems of immune response = not being able to splice things correctly  Fig. 17-8 Igg can bind to two different antibodies that are identical  -can cross the placenta = small enough to do that -when we see antigen for first time = first see IGM = large complex of five  separate monomers brought together through J chain -first time I see antigen = make an IGM response = switch over to IGA  -IGM being so big = never gets out of blood = can’t get to tissues = that’s  why we switch from making IgM initially and switch over to making IGG (can get out of blood and get into a tissue where it’s needed) -IGM is also a monomer = only one unit outside of B cells -not only is made to respond to an antigen, also serves as a  receptor/recognizing molecule on the B cell = see the particular antigen = immune  response -IgD = not quite sure what it does = it is also attached on outside of B cell =  not really acting as receptor like IgM -IgA = usually is joined by a secretory piece, a protein, see 2 different  antibody molecules brought together = secretory IgA = lining all of your openings to outside world (nasal passages, urinary tract, any mucous lining membrane) =  exactly where you’d want the antibody = where we take in a lot of pathogen -also have nonsecretory IgA = predominant is secretory-nonsecretory = being localized in secretions and in the mucous  membranes -IgE is involved in Allergies -doing something with worm type infections -culprit of allergies Table 17-4 Properties of Antibodies -out of all 5 classes = only IGG goes across placenta to fetus Fig. 17-9 -B cell is stimulated so the IgM on B cell sees antigen = ultimately start expanding  out B cell  -for this to happen = we have T helper cells = knows this is the B cell it can  help = because it is displaying the antigen to the T cell that can respond to the  antigen -t cell secreting lymphokines= allowing b cell to mature into IgM = plasma  cells -over a few days = have IgM for particular antigen = means that it is the  primary response = all of a sudden over days = stop making IgM = now switch over to IgG = the antigen binding variable region gets attached to the constant IgG  region = Class switch  -the reason is because IgM can’t get out of blood = Igg can get into  liver and react with pathogen directly there -t helper cells are helping this class switch -what’s the concentration of antibody in the sera (the fluid portion of blood  minus all of the cells in blood)? = antisera = antibody in sera -making memory cells as well as plasma cells -the next time you see same pathogen = anamnestic response (secondary) -the second time around, memory cells get stimulated = have IgM that see  antigen = ultimately start mounting an immune response quicker = have total  antibody responding faster and dramatically = still make IgM first = not as first time around = switch faster = make more antibody faster  -need T helper to get to memory and for the switch What are T helpers doing? Fig. 17-9 T dependent cells are the predominant immune response = most B cells do need to  T help-the B cell has a monomer of IgM on its surface = that’ show it knows that  variable region of the IgM recognizes that specific antigen  -the B cell has this antigen attached = will display on its surface the antigen  another protein = MHC 2 = a protein that’s on surface of lymphocytes = is hanging  onto the antigen and displaying it on its surface = so that T helper cell can  recognize that antigen being displayed -the t helper cell has a protein that can recognize a specific anting in  conjunction with a specific MHC protein -B cell displaying MHC2 and antigen  -the helper cell immediately responds by making cytokines = allows B cell to  = clonally expand = differentiate into plasma producing cells = t is also secreting  lymphokines = to remind b cells to store and make memory cells -t helper cells also proliferate and ultimately not only do they secrete  lymphokines directing b cells, but they also go into memory = need both of them =  can’t wait for t cells to respond a second time =why both attributes apply There are some antigens that don’t need a response that is T cell depending T independent antigens -the B cell independently can recognize that antigen = don’t need help = can  go on and mature = antibody secreting cells = these T independent B cells never  class switch = can only make IgM = never have memory because there is no help  from T helper cells Acquired immunity has to respond to antigen in a specific way = these  antigens don’t require b cell memory or t helper  -are very good repetitive strut res like carbohydrates = just need to mount an immune response that’s an IgM = not concerned with class switching -majority of response to antigens are t dependent  -infected with HIV = not only do t helper cells get destroyed = ability to make  antibody response = severely compromised = b cells don’t get t helper cells they  need = affect humoral and cell mediate immunity Wed = talk about how antibodies work? And T cells and antigen reactions during  allergiesApril 19, 2017 T-dependent antigens require help from T helper cells -help B cells -B cell has a monomer = IgM = recognizes specific antigen that it can  respond to -antigen gets presented on surface with MHC II protein -signals T helper = responds to that antigen = will secrete lymphokines, or  interleukins, or chemokines = the B cell can start maturing and expanding its  population (clonal expansion) -mature into plasma cells = secrete antibodies -T helper cells release factors = to create B memory cells and IgG (can go out of blood and into tissue where infection may be) -you have T helper memory cells = respond much faster with a stronger  immune response Fig. 17-10 IgA, Igg, and IgM can do any of these -the IgA is going to pick up this particular toxin = once in circulation = the antibody  can grab onto the toxin before it has a chance to grab onto the host cell -the macrophages can readily see the constant region of the antibodies =  toxin is destroyed -neutralization = neutralizing toxin = taking it out of circulation = no chance  to enter host cells Ex: viral infection = make an antibody to the virus = grab the virus out of  circulation before it has a chance to bind to receptor on the cell -can have neutralization with an IgG and even IgM can be involved in  neutralization reactions -b) the next one is having antibody that decorate an antigen = make it readily seen  by macrophage -once antibody binds to pathogen = decorated with all these antibodies =  opsonization -macrophages have a receptor for the constant region on the antibody =  phagocytic event -another way how antibodies respond to pathogen c) IgM (large complex, 5 monomers brought together = can pick up 10 identical  antigens) = can grab onto a particular pathogen or antigen = decorates it = very often is readily picked up by complement (not mutually exclusive) once C1 can bind  to antibody attached to antigen = whole cell will undergo lysis and ingestion once  last components of complement occur Fig. 17-11 Overview of how B cells make antibodies -mature in Bone marrow -any made in fetal development = clonal deletion of B cells that produce antibodies  against self -now that we have B cells, we know we have the diversity, specificity -Find that pathogen by being presented with that particular pathogen by  macrophages -macrophages and dendritic cells can present pathogen to B cells -macrophages (APC) as well as a cell that can digest a pathogen -once the B cell is stimulated = seen antigen it can react to = B cell will need help  from T cells -it’s going to take that antigen = display it on MHC 2 complex = T helper cell comes  to help -T helper cells help B cells to mature and express antibodies out of their plasma  cells -antibodies = neutralization, opsonization, cell lysis Monoclonal antibodies -an antibody is very specific for a particular antigen -involved in tumor surveillance  -scientists realized that antibodies really have a major role in health not only  for treating infectious diseases = also surveillance for abnormal growth -problem = needed enough antibodies for a clinic = not only would you want  enough antibodies = want it to be very specific for the antigen Scientists (1970s) wanted to have one specific antibody = “magic bullet” = was  going to be able to have the specificity to a tumor cell and it was going to deliver a  toxic payload (wanted to put some of the toxins, diphtheria, tetanus, was going to  be a toxin or a radioactive molecule) and that was going to be the silver bullet -so now you have specificity of tumor cell = can deliver toxins  -by having specificity and delivering toxic payload = directed way of treating  tumors-looking to get that specific antibody response = delivering a toxic payload =  using T cells to be involved = and kill specifically tumor cells = to do that = needed  a pure antibody/monoclonal antibody Fig. 17-12 Developed a procedure to make monoclonal antibodies Injected an antigen of interest into a mouse -lymphocytes respond to antigen = expressing B cells -wanted to make sure that they had an ability to produce as much antibody as  possible -used myeloma cell line, if they could fuse the lymphocytes with this continuous cell line = ultimately find a cell line expressing the antigen responding antibody that  was going to be growing indefinitely  -ex: strep A = monoclonal antibodies used = clinical settings  Fig. 17-13b T cells respond to antigen on surface of macrophage (APC)  MHC 2 protein is sitting on surface of lymphoid cell line and macrophages -any T cell that can respond to that particular antigen = will become activated = will see interleukins/chemokines released by the cell that will activated the T helper  cells = will be turned on to make another chemical called IL2 = will set these T cells  in motion to propagate -either mature into TH1 cells (Delayed hypersensitivity) = help macrophages  that are harboring things like mycobacteria and Yersinia pestis = secrete all sorts of  factors to attract more macrophages and make it work a little harder to produce  toxins = to get rid of pathogens = respond and release chemicals/cytokines to try to get infected macrophage killed with whatever is inside =TH1 cells are involved in a lot of allergic responses which are delayed (ex: poison ivy compared to peanuts) -involved with allergic reactions like antimicrobial agents = what these  T delayed hypersensitivity cells -also have TH2 cells that have its display of antigen = respond to B cell =  matures = releases antibodies = humoral immunity against foreign antigen -HIV infects T helper cells = recognizes specific receptor on T helper cells =  not only are T helper cells depressed in someone = not only do you hurt the T cell  response = ultimately destroying humoral immunity = immunocompromised =  inhibiting ability to make antibodies Fig. 17-13 b Cytotoxic T cells-antigen present to T cytotoxic T cells -have an MHC 1 protein on all of our cells -you have antigen sitting in pocket of MHC 1 and cytotoxic T cell sees antigen = cytotoxic cell goes through multiple divisions -the Tc cell will look in body for any cell that has antigen displayed (tumor  cell, rickettsia, chlamydia) = makes direct contact = releasing factors (perforin) =  gets released from cytotoxic cell = causes a whole in this aberrant cell and dies -NK cells are in the lymphoid cell line (have markers) = do not need to be  presented with an antigen from a macrophage = can respond directly to any  aberrant cell in our body that’s displaying an antigen in the pocket of MHC 1 which  is on all of our body cells -don’t need to be presented with antigen -stimulated because there are chemicals being released (interleukins,  chemokines) -that’s why cytotoxic T cells are different = but Tc does the same thing  that an NK cell does -T cells are part of cell mediated immunity = cell is coming up to infected and responding unlike B cells releasing antibodies = attaches to particular antigen Fig. 17-15 T regulatory/suppressor -have to be presented with antigen via macrophages or B cells that need their help  = T cells can mature once activated: -into T helper cells = help B cells T helper cells = can help macrophages (Th1 and TH2) -APC through the MHC 1 complex through the cytotoxic cells -NK cells don’t respond to Antigen presenting cell  Once you mount an immune response = need to shut off immune system  Ex: leukemia = where your regulatory T cells are involved  -T cells are made in very small amounts, very difficult to study them -the T cells that are suppressor = play a role in regulating = trying to  regulate everything = mounting a health immune response Good diagram of explaining everything Table 17-5 B cells, T cells, and Macrophages -B cells have monomer of IgM -T cells don’t have antibody = have receptor protein to see antibodyFig. 17-17 Good summary This chapter = see tables of different types of vaccines and what’s in the vaccine =  not going to ask about vaccination schedules  Should look through rest of chapter = define things like sera (fluid part of blood  containing antibody = antisera) This is what would happen if you got a viral infection Virus enters us = things in our innate immunity that can take care of virus -interferons, coughing response, trap in mucous membrane of respiratory  passage that may grab this virus before it has chance to get established -mucous membranes and openings to body has IgA = grab this virus and pull  it out before it enters into cell If in circulation, have circulating antibodies to take care of virus If it enters liver = liver infection = have cytotoxic T cells now displayed on this liver  cell is antigen from virus = Tc can see and destroy this -also have NK cells to take care of this cell Some types you get chronic infections (hepatitis) -because they constantly have a virus and calling in NK cells and Tc cells =  damage to healthy tissue = inflammatory response = releasing a lot of factors =  cell death -unfortunately, people who have chronic infections = that organ that’s  infected = allowing for an inflammatory response -chronic inflammation allowing immune system to do collateral damage =  trigger an overgrowth = cancer  Chapter 18: Immunological Disorders -figured out how our healthy immune system works -What are they? Inappropriate or inadequate immune responses -allergy “hypersensitivity”: immune system reacts inappropriately to a foreign  substance -getting signs and symptoms of an inappropriate reaction = can be life  threatening = anaphylactic shock -immunodeficiencies: primary or secondary -primary: born with it  =missing complement factors, people that have problems with  bringing the heavy and light chains together (missing enzymes), missing healthy B  and T cell response = the boy in the bubbleFirst type of sensitivity: immediate Type 1 Hypersensitivity -within seconds developing signs and symptoms Fig. 18-1 IgE is a class of antibodies in helping inflammatory response (cuts, wounds) = we  want mast cells and basophils to be releasing factors -unfortunately don’t want it to be involved with allergies but it is -why people are allergic is not understood -an allergen comes into our body = macrophages will bring it in = digest it =  present it to B cell = B cell will display that antigen on its surface = this antigen will  cause the B cell do the class switch to IgE = will mount an IgE response -on outside of basophils and mast cells is a receptor that binds to the constant  region of IgE =these basophils and mast cells will grab onto constant region and  display them on their surface First exposure = IgE placed on surface of mast cells and basophils 2nd time= now you’re primed to make a lot of IgE = picked up by mast and basophils = as the antigen grabs onto the antibody = IgE molecules start congregating =  grabbing onto antigen = stimulates the mast and basophils to release chemicals =  histamines cause blood vessels to dilate and get leaky -pollen = developing mucous in lungs -can start getting constriction = leukotrienes = asthma like response to  allergen  -ultimately that’s what causing all those signs and symptoms  -IgE triggered mast cells and basophils which triggered all those signs and  symptoms -this is your typical immediate type 1  Table 18.2 Some mediators of Immediate hypersensitivity and their effects Can go into anaphylactic shock  Fig. 18-5  a) normal allergic reactions -making IgE = causing mast cells and basophils to be released b) desensitization = block this type 1 sensitivity -done under supervision -try to introduce the allergen into a different part of your body (ex: pollen) =  introduced underneath your skin = could potentially go under anaphylactic shock, needs to be monitored = hoping that looking at this allergen in a different format =  introduce the allergen = instead of making IgE response = will make a normal  immune response = IgG will grab onto allergen in the future/neutralizing antibody = if you ever breathe it in = IgG will grab it out of circulation before it gets to mast  cells and basophils -trying to have your body to make blocking antibodies/neutralizing = grab the toxin out before the IgE has a chance to grab and see the allergen -hope that the T regulatory cells may be stimulated -by seeing antigen in a different format = stimulate T regulatory cells =  hoping will react with B cells that make IgE and stop that -trying to do 2 things = some success with this method -where we get to see the T regulatory cells = secreting factors into B cells =  can’t make IgE = preventing it from making IgE Table 18.3 The ABO Blood Group -example of cytotoxic Type 2 Hypersensitivity -antibody that we could make destroys the cell -ex: blood typing  -referring to a carbohydrate on surface of blood cells Type a: a carbohydrate Type a: b carb Type ab: a and b on RBC O: don’t have either carbohydrate -in our serum = RBC with A carbohydrate = good chance I have anti—B  antibodies = would respond to B carbohydrate on B blood AB = neither anti A nor Anti B  O person = doesn’t have either carbohydrate = have both types of antibodies -any AB person = person that could take any type of blood = don’t have any  antibodies to the carbohydrates on the RBC = O person is the universal donor -carbohydrates being very similar in structure = look like normal carb on  pathogens = chances are I have seen a b carbohydrate and have responded to it Fig. 18-6 IgM will decorate that RBC -phagocytic cells will come in -agglutination = carbohydrate is decorated with IgM = big complexes form -either that mistype blood will get destroyed through phagocytosis or will trigger  complement cascade = lysis  -causing sever abnormal reactions in our body -you also type a protein on the outside of RBC Rh protein  Fig. 18-8a Rh refers to positive or negative -if woman doesn’t have Rh protein = or if baby is Rh positive = during first baby =  inevitable mother during pregnancy will see baby’s blood = woman will immediately start making an immune response = she will then have Rh antibody response in the  future -the first baby shouldn’t have a problem as far as woman making anti Rh  antibodies -the baby’s blood isn’t seen by mother until late in pregnancy -problem is during next pregnancy = if I have Rh b cells responding to Rh  protein = slowly through circulation = since IgG can cross placenta = can damage  baby’s fetal blood = when a woman is Rh negative = will give her passively  antibody close to delivery to Rh protein = will pull baby’s blood out of circulation =  not have mounted an immune response to that Rh positive baby Ex: passive immunization -rogam grabs baby’s blood out of woman’s circulation -why can’t we worry about baby’s protein type = IgG can only cross the  placenta = the carb is an IgM response = example of a T independent immune  response = don’t do the class switch = IgM can never cross the placenta = don’t  have to worry about what type of blood the baby hasApril 24, 2017 Alternate room for exam on May 5, 2017  Review Next Monday May 1 1. Monocytes, macrophages, dendritic cells 2. antigen, or pathogen 3. IgG antibody has two arms = 2 identical antigens 4. 2 things that T helper cells help B cells -help cells to proliferate (clonal expansion) and differentiate into plasma cells  to form antibodies = help with class switch, and help them form memory B cells Fig. 17-9 Hypersensitivities w-th type 1 = immediate hypersensitivity  -have IgG = immediate = start showing signs and symptoms Type 2 Cytotoxic = antibody is reacting to something on the cell = Ex: blood typing for carbohydrate and Rh factor Tonight: Immune Complex Hypersensitive -overabundance of antibody and antigen complexes -macrophages can’t clear them fast enough -can’t get them through phagocytosis fast enough = go to organ = or blood  vessel wall = nonspecific deposits -wind up having complement recognize the constant region of the antibody = set off complement cascade = inflammatory response -to many immunocomplexes = triggers inflammatory response = visualize a  lot of destruction in that area (blood vessels, organs) -giving passively antibodies to that infectious agent like diphtheria  -when you give people passive antibodies (from animal) = the antibody looks different from human antibody = given enough of this = mounting antibody  response to antibody = called anti-antibody = resulting in serum sickness = having antibodies reacting to passive antibodies getting to treat infection = not treated  anymore = not treated like this unless bitten by snake = to treat an infection =not  happening -autoimmune disease = making Antibodies against own tissues =  would see this type 3 disease = mounting ab response = not being cleared fast  enough = destroying the cells that are being bound with that ab = causing a lot of  this inflammatory type reaction-when you look at hypersensitivities = what is happening?  -as soon as you see the ag bound with ab = complement cascade,  histamine being release, macrophages = causing signs and symptoms = tissue is  getting damage usually when you have these hypersensitivities = trying to clear  pathogen Fig. 18-10  Receiving antigen underneath skin = will see location of ag injected = set off  complement cascade = attracting neutrophils and the complement (one of those  factors is causing histamine release) = all happening where ag is injected =  ultimately these complements start attaching to these walls = damage to the tissue -these hypersensitivities all involve antibodies Type 4 = cell mediated or “delayed hypersensitivity” -involves T cell reaction (Fig. 18-12) -MHC 2 present APC = calling T helper 1 cells = present antigen to t helper 1  = secrete cytokine = help macrophage digest whatever pathogen that is = usually  this delayed hypersensitivity =by the time you get presentation of ag and  macrophages are getting help from TH1 to make macrophage work harder, cause  macrophage to slough off so they don’t leave site -T helper are working with macrophage to kill that ag (granulomas,  tuberculosis, gummas) -when the t helper cells are trying to get rid of that pathogen = start  calling the factors = see necrotic tissue because there are a lot of macrophages at  that site -but this is a delayed response (ex: allergic to poison ivy, oils from that  eventually get presented to the T helper cell by the ag presenting macrophage =  start developing an itchy skin, redness, swelling, all the symptoms = doesn’t  happen instantaneously like peanuts having type 1) -TH2 help B cellsApril 26, 2017 Chapter 15 Epidemiology: study factors involved in the spread of disease. Look at relationships  among the host, microbe and environment. -involved with following diseases like cancer in a community, interested in microbe  and how we are exposed to the agent Etiology: cause of disease KNOW THE TERMS (BOLD WORDS) Epidemiologists = (unsung heroes, reporting to CDC) Ex: EBOLA, Zika virus, don’t know how organism is being spread, go into war  torn countries Fig. 15-1 Tracking number of infectious agents over a period of time -when encountering first case = incidence disease -looking at a population of 100,000 people  -people are always looking to see if this incidence for this disease is increasing -is there going to be some sort of an epidemic in the environment -over course of person’s infection = get included into the prevalence of the disease  in the community = until they are recovered = scored in the prevalence (potential  spreaders) Disease Terms -Morbidity rate (# affected by disease) versus mortality rate (# of deaths due to disease) -Endemic = disease agent always present (ex: cold or mumps virus) -Epidemic = higher incidence number than normal (ex: flu season, want to prevent  having an outbreak) -Pandemic = worldwide epidemic (ex: zika virus) Fig. 15-7 -can isolate factor on a particular cruise ship = common-source outbreak Ex: all ate that particular salad, those that didn’t eat didn’t get sick -propagated epidemic= people who always have agent but don’t know it Reservoirs1. Carriers (inapparent infection) -people can be carriers of an infectious agent (don’t know they’re spreading  it) 2. Animal (Zoonoses) Ex: rabies are in many different animals (getting them vaccinated) Ex: bubonic plague, Yersinia pestis 3. Non-living = soil, water, food -loads of organisms = or endospores in that soil -if skin is breached = cut = contamination with soil = chances that cut could  become infected -water: quality of water (ex: protozoal diseases) -food preparation = keeping things clean, uncooked food Ex: zika virus, where is it when there is no outbreak? -Disease organisms can enter us through any opening in the body (like the mouth),  broken skin, hair follicles (ex: folliculitis), insect bite (ex: not only injecting infectious agent, but mere bite leaves opening in skin), placenta (ex: zika virus). -Diseases can exit the body through bodily fluids, including mother’s milk, dead skin cells, and fecal material.  Fig. 15-11 Vehicle Transmission Contact transmission -Direct Contact = bat that has rabies -Droplets = coughing, sneezing = organisms present Indirect contact = by soil organisms or fomites Vehicle Transmission: -waterborne -airborne: dust particles -foodborne: toxins causing food poisoning Vector Transmission (flies, fleas, ticks) -Biological vector: being bitten or exposed to vector who is exposing you then to the infectious agent Ex: Yersinia pestis, the tick that gives you Lyme disease,  -Mechanical vector: flies sitting on top of sandwich-allowed to transfer infectious agents from one area to something that the  human WILL be exposed Fig. 15-12 -best practice to cover your mouth when coughing -better to cough in arm Fig. 15-13  Herd Immunity: has to do with why vaccines work -would like to immunize at least 90 to 95 percent of population = not  spreading infection -half of population = little outbreaks -have that one person with infection (50/50 chance) -if you look at number of cases in community = 50/50 chance -organism present in community = chance -enough people that are still susceptible -90% of population immunized -smallpox was 100% vaccinated -working on polio -chance of infectious person ever getting to susceptible person isn’t all that  great -the herd is the human population that is vaccinated = protecting those that have  not received the vaccine How To Control Disease -Isolation -when you know they are sick -Quarantine  -difficult to do -when you suspect someone to be exposed = potential incubation stage =  would like to see them not in the community = stay in house = not come out in  public until sure they are passed incubation stage until they’re healthy -exposed = like to see them out of community until you are sure they do not  have the sickness -Immunization-Vector Control -harder to do in poorer countries if you know infectious agent is in a  population of animals -Organization like the CDC and WHO monitor disease outbreaks and set up  programs to support health Fig. 15-17 Keeps people informed Fig. 15-19 Preventable deaths -It is estimated that the majority of deaths from infectious diseases can be  prevented with existing, cost-effective strategies Childhood vaccinations have proven extremely effective in reducing deaths from  measles and have other preventable diseases Bednets, screens and other prevention and treatment strategies can prevent 50% of all malaria deaths -all types of programs to help people take their medicine = DOTS -rotavirus = a lot of children die because they never get rehydrated = poor  countries = babies die = program to try to help poor countries (IMCI) -Antibodies used passively -HIV prevention strategies such as condom promotion, sex education and  treatment of STIs have been proven to reduce the spread of HIV/AIDS. Fig. 15-20 Common organisms causing infection  -exogenous: hospital personnel not washing hands -endogenous nosocomial infection: coming from you -all these organisms are in you Table 15-5 Some Important Universal Precautions and Recommendations from CDC -worst place to be sick is the hospital -so many antimicrobial agents = high degree of drug resistance -wear gloves and gowns if soiling of hands, exposed skin, or clothing with blood or  body fluids is likely. Fig. Pg438-hope that people are sanitizing the correct thing especially with all the invasive  procedures Ex: colonoscopy  Fig. 15-23 Exposed to an organism that we may not be exposed to = through a surgical wound = major area exposed  -urinary tract = catheterization = tears in epithelial lining -respiratory tract = dust we can’t see -needles = into blood -it’s no wonder that in a hospital = want to get in or out as fast as possible Epidemiologists have to be concerned with the risk of bioterrorism = have to be on  guard because we see how organisms are our friends = can use pathogen for  malignant purposes Ex: CDC reports For Exam 4 =go back and study al fungal and protozoal organisms, know all  immunology (innate immunity, the serology = how we use antibodies to make a  diagnosis) -know chapter on epidemiology -short answers, m/c, matching -typical 80 min exam

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