MIC 320 Exam 3 Study Guide
MIC 320 Exam 3 Study Guide MIC 320
Popular in Introduction to Microbiology
Popular in Department
verified elite notetaker
One Day of Notes
verified elite notetaker
verified elite notetaker
verified elite notetaker
verified elite notetaker
One Day of Notes
verified elite notetaker
This 15 page Study Guide was uploaded by Serena Buckley on Friday March 6, 2015. The Study Guide belongs to MIC 320 at University of Miami taught by Roger Williams in Fall2012. Since its upload, it has received 74 views.
Reviews for MIC 320 Exam 3 Study Guide
Report this Material
What is Karma?
Karma is the currency of StudySoup.
You can buy or earn more Karma at anytime and redeem it for class notes, study guides, flashcards, and more!
Date Created: 03/06/15
Exam 3 Immunology Why do we need an Immune System Acquired Immunodeficiency Syndrome AIDS Human immunodeficiency virus HIV infects human Tcells macrophages and dendritic cells via cell surface receptors Primary Severe Combined lmmunodeficiency absence of functional T Iymphocytes leading to a defective antibody response Most severe form of primary immunodeficiencies Victims are extremely vulnerable to infectious diseases The boy in the bubble 19711984 lived in completely sterile environment Died because he received a bone marrow transplant containing traces of dormant EpsteinBarr virus Pathogen replicating organism that causes disease Immune system comprises the cells and liquids in the body that are dedicated to defend pathogens lmmunity comes after the infection Capacity to specifically protect not fight against the original pathogen Diverse Living Agents that Cause Infections a Human immunodeficiency virus HIVthe cause of AIDS b Influenza virus 0 Staphylococcus aureus a bacterium that colonizes human skin is the common cause of pimples and boils and can also cause food poisoning d Streptococcus pyogenes the bacterium that is the principal cause of tonsillitis and scarlet fever and can also cause ear infections e Salmonella enteritidisthe bacterium that commonly causes food poisoning f Mycobacterium tuberculosis the bacterium that causes tuberculosis g Listeria monocytogenesa bacterium that can contaminate processed food causing disease Iisteriosis in pregnant women and immunosuppressed individuals h pneumocystis carini opportunistic fungus green in the lung iepidermophyton flooccosumringworm fungus j candida albicans fungus that forms opportunistic oral and genital infections h trypanosoma brucei African sleepy sickness I Schistosoma mansoni causes schistosomiasis Parasites that are found in the blood vessels of the host Extracellular or Intracellular Living Agents that cause infection Extracellular located in interstitial spaces blood lymph and epithelial surfaces Viruses Bacteria Protozoa Fungi Worms Gonorrhea Strep Cholerae Worms lntracellular Cytoplasmic and Vesicular Viruses Chlamydia Rikettsia Protozoa Mycobacterium Yersinia petsisis Legionella pneumophilia Cryptococcus neoformans Leishmania Extracellular or Intracellular Living Agents that Damage our Route orientry Mode of transmission li39lucosall surfaces Inhalation or ingestion of infective materiall Mouth a quotd Ieg sa live id roplletsi respiratory tract Spores Contaminated V water or food Gastrorntestlnal tract Sexuai tranzirrriissionlI Reproductive tract 7 infected bioocl arid other to lites Opportunistic pathogens lResid errt m icroiairota Bzesidlent microbiota Externai epi leiiza External surface contact Minor skin abrasions Pluncture wotinds animalls 1wounds and abrasions Musiqliuit l bites Medias I ctb39t I152 3935 Deer tickhites lili fi f ii i1fri3912iiiBjrii iaiF f t EB Pathogen Measies virus virus Va ricelllazoster in uenzae Neis serio Baciiiu s anthmcis Hotauirius A Saimoneiio enteririd is S Fibrin chuoiercre B virus lHiu man vi ru 5 Neisseria Candida nibicans Bacillus anthracis Ciosrridium tetnni Froncis eiiu tuiorensis i lav ivi ru 5 Borreiia Pias39m odium spp Figure 22 Janeway s lr39rrrrrIurtoizriollngyj Beth Garllartd Science 201 2 Mea slles Mononucleosis Inhalation anthrax Dia rrhea Jla u ncI ice Food poisoning Chollera fever lB Acquired Gonorrhea 39CanIzllidiasirsjr thrush Pneumonia Athlete39s foot Cutaneous anthrax Tetan u s 39ll39ula remia r39el low fever disease M aiaria Type oi pathogen bacteriu m bacterium bacterium Rotaui runs lF icorinavi ru 5 re mnegative bacterium bacteriu m bacterium Retrovirus bacterium Bacterium bacterium bacterium bacterium Virus Batter i u m Protozoan Extracellular or Intracellular Living Agents that Cause Disease Exotoxiin e a Direct production Endotm m cytopathiic effect Pathogenic mechanism Streptococcus Escherichia caii Variolla pyogenes Haemophiius Varicelllaazuster Staphylococcus in uenzae Hepatitis B virus aureus Salmonella typhi Polio virus quot55th Corynebacterium Shige a Measies virus agent diphtheria Pseudomonas influenza virus Ciastridium tetani aeruginasa Herpes simplex Vibria choierae Yersinia pestis virus Human lherpes virus 8 HHVBI Tonsil39itis scarlet Gramanegative Smallpox fever sepsis Chickenpox IBoills toxic shock Meningitis shingles 39 WmnleF pneumonia Hepatitis Dlsease food poisoning Typhoid fever Poliomveiitis Diphtheria Bacilllary dysenteryi Mga iesrf39lflb acute Tetanus Wound infection S CIeFDS Ing 39 Chellera Plague VP a39iei QE Pha39M39s llnfluenza Cold sores Kaposi39s sarcoma Figure 24 part i of 2 Janeway39s immunobiologyi Bed i Garland Science 2011 2 Qualities of the Immune system 2 IMPORTANT EXAMPLES Macrophages and neutrophils against extracellular bacteria in phase 1 and in phase 2 antibodies made by Bcells Natural killer cells against intracellular pathogens in phase 1 and in phase 2 CD8 Tcells degranulalion phagocytcsis mast celllll macrophage natural killer basophii eosintophil neutrop hil active Nit cell neutrophil a inlectecl cell tht39mtc 39 E 7 tthymi c cortical medullary immature dendritic celli antigenapresenling follicular endothelial epithelial goblet atpoplotit epithelial cell epithelial cell dendritic cell ceil AFC dendritic cell cell ceit cell cell T celi activated B cell plasma cell antibody antibody pentameric T cell lgG Ing ligA lglttt lgE QM i i 391 139 7639quot quot Tcell 39 receptor antibody antibody production dirneric IgA protein antigen imp mute Epithelial cells control the process of clot formation and maintain vascular tone They are normally at rest but in the lymph nodes they form the High Endothelial Venuoles HEV Specialized structures designed to attract Tcells into the node Locally secreted cytokines alert endothelial cells to danger Neutrofils make up granulocytes with eosinophils and basophils Grow in bone marrow and are released into circulation Uses granulocytes for phagocytosis Natural Killer part of the innate immune system Is a lymphocyte along with Tcells and Bcells Does not have any antigen specific receptors and is considered a large granular lymphocyte Is very similar to toxic Tlymphocytes Does not kill normal cells because it detects MHC1 molecules Plays a very important roll in early infection detection Immature macrophage garbage disposal of the immune system Grows in the bone marrow into a macrocyte Binds to invaders and makes cytokines to activate vascular epithelial cells Potent phagocyte Modulates responses for adaptive immune system Modulates adaptive response Dendritic Cells very rare Presents antigens to Tcells resulting in the development of a primary immune response and immune memory Once it is in tissue it is immature Notifies lymph nodes of infection Migratory skill serves as a link between the innate and adaptive immune system B Cell born in bone marrow Couples with helper T cells and cytokines in follicular lymph cells to mature and secrete antibodies into the lymph Can become a memory cell and travel to lymph nodes or bone marrow or a plasma cell T Cell travels through the blood to the lymph cell to be activated by a dendritic cell Chemokines signal B cell to be released from the follicle The immune system can have some negative repercussions Rejects vaccinations transplants causes allergies and immunodeficiency Serum fluid component of blood after the clotting proteins and cells have been inactivated or removed Contains fluidsoluble components of the immune system Can be transferred to other individuals to provide passive immunity Prevention is better than a cure Lysozyme in tears and other secretions dissolve cell walls Flora in mouth compete with pathogens Cilia in nasopharynx remove particles and microorganisms Mucus in cilia lining of the trachea move particles out of the body Antimicrobial fatty acids on skin Provide a barrier pH in gastrointestinal tract inhibits microbial growth Skin Gut Lungs Eyeslnosel oral cavity Epithelial cells joined lay tight junctions Longitudinal flow of air or fluid Movement of mucus by cilia ili39ears Nasal cilia Pulmonary LOW PH surfactant Enzymes in tears Fatty ands and sallva lysozyrne Enzymes pepsm Bdefensins otdefensins Lamellar cryptdins i tatdefensins Histatins bodlies Reglll lecticiclins 1 Cathelicidin Bidefensins Catl1elicidin Cathelicidin Normal microbiota Figu re 26 Janeway s lmmunoblology Bed l Garland Science 2012 Innate immunity Recognition by immediate Infection plgformed non39 Hallow Of 04 hams 39 speclflcand broadly v Infectlous agent speci c effectors Early induced Recruitment Recognition of PAMIPS I Rem al of innate response Infection of effector Activation of effector inf ctiglrs a em learly 4 96 hours cells cells and in ammation 9 Adaptive immune 7 Transport of Recognition Clonal expansion 7 Removal of response Infection antigen to by naive and differentiation 7 infe s 39a m llate gt96 hours lymphoid organs B and T cells to effector cells 9 Figu re 21 Janeway s Immunoblology Bed 92 Garland Science 2012 Immune Barriers Antimicrobials preexisting weapons made by nonimmune cells Lysozyme digests the wall of the bacteria Defensins antimicrobial peptides secreted by epithelial cells Disrupt the bacterial membranes by pores the skin and lung activity Cryptins defensins made by the paneth cells of the small intestine Reglll made by Paneth cells Kills grampositive bacteria Lamellar bodies defensens packaged in granules Released by Cathelicicins contained in lamellar bodies Disrupt membranes Histatins made by the glands in our mouth and exhibit fungicidal lnfection the invasion of a host organism by disease causing organisms pathogens their multiplication and the reaction of the host to these organisms and their toxins immune response Innate immunity different preexisting or quickly available mechanisms to defeat pathogens Do not increase after rechallenge Adaptive immunity needs time to be stimulated after the exposure to a pathogen Exquisiter specific Leads to memory cells providing immunity which helps respond the second time much more vigorously Phagocytosis Macrophages large phagocytic leukocytes of the innate immune system Eat extracellular bacteria and the corpses of dead eukaryotic cells Have phagocytic receptors that bind microbes and their components The bound material is then internalized in phagosomes and broken down in phagolysosomes Complement Proteins Comprise Soluble PatternRecognition and Effector Molecules Tolllike Receptors TLR comprise an ancient family of pattern recognition molecules on the surface and in the cytoplasm of phagocytes esp macrophages PathogenAssociated Molecular Patterns PAMPS repetitive structural components of pathogens How the TLRs sense danger and activate cells Cytokines proteins that affect the function of other cells Made by lymphocytes that are called interleukins Chemokines proteins that stimulate the migration of phagocytes and other cells of the immune system lL1B activates vascular endothelium activates lymphocytes destroys local tissue increases access of effector cells causes a fever and produces lL6 TNFa activates vascular endothelium and increases vascular permeability which increases entry of lgG complement and cells to tissues and increased fluid drainage to lymph nodes fever mobilization of metabolites and shock lL6 activates lymphocytes increases antibody production fever and induces acutephase protein production CXCL8 Chemotactic factor recruits neutrophils basophils and T cells to the site of infection Neutrophils large polymorph appearing leukocytes of the innate immune system Phagocytic and are characterized by cytoplasmic granules loaded with degradative enzymes and a segmented lobular nucleus Most abundant type of white blood cells Summoned to site of infection by cytokines and chemokines Macrophages and Neutrophils Execute Similar functions Process of Inflammation lnflammation the local accumulation of fluid plasma proteins and white blood cells that is initiated upon an infection or local immune response Results in erythema redness edema swelling heat and pain Local Inflammation especially TNFa stimulates blood coagulation in order to contain pathogens clots Systematic lnflammation results in shock and BIG blood clotting followed by bleeding Systemic edema causes decreased blood volume and collapse of vessels Disseminated intravascular coagulation leads to multiple organ failure and death Dendritic Cells DC characterized by long projections When activated they pick up pathogens or destroyed pieces of pathogens at the site of infection and travel via the afferent lymphatics to the draining lymph node Here they are capable to potently function as antigen presenting cell This initiates adaptive immune responses by B cells andor Tcells Serve as a bridge between the lnnate and adaptive Immune response Antibodies Ab produced by Bcells in response to infection or vaccination as a part of the adaptive immune response Have a unique structure at one end to recognize the pathogen but share similar structures at the other end the Fc portion Specifically bind to the epitope of the antigen a specific portion unlike complement and TLRs Antibodies Fight Extracellular Pathogens by Three Means Specific antibody 2 A LIA 1quot 1quot Santana ml extracellular space 39 I i Bacterial toxins Bacteria in pllaslmla Imacrophagle I P 7 receptors 391 for toxin r 397 H 17 Opsonizatiun Cxalmlplemlenit activation V V lllngest ion by Ingestion by macrophage macrophage Figure 1125 Jameway39s llmmwmubiulogyr Eedl to Garland Science 2m 2 Negative Selection During Bcell Development and Tcell Development Comprises One Mechanism to To Avoid Self Reactivity Innate and Adaptive Immune systems The Spleen Acts as the Draining Lymphnode for the blood Plasma Cells where Bcells are created with the help of cytokines released by Tcells Plasma cells that live forever provide memory for specific Bcell response Bcell Memory can be Measured by Determining Antibody Titers T cells recognize Antigens by first breaking down the antigen into peptide fragments binding the epitope peptide to a MHC molecule and the Tcell receptor binds to both the MHC molecule and the epitope peptide Dendritic Cells chop up antigens to present them to Tcells Activation of Bcells class II B cell Figure 31 3 The Immune System 3ed CC Garland Science 2009 MHC molecules display peptides of an antigen for their recognition by Tcells Human MHC is known as KLA Principle determinants of acceptance or rejection of tissue grafts between individuals There are 3 biallelicly expressed class 1 and class 2 genes Polymorphism indicates that genes exist in a variety of versions different alleles each of which is present in a different individual MHCHLA comprises the most polymorphic gene cluster in humans Superantigens overpower the immune system They bind to a common region of MHC II and to 530 of all TCRs Class 1 MHC Class 2 MHC 3x2 different gene loci 6x2 different gene loci interacts with CD8 interacts with CD4 presents intracellular presents extracellular antigens antigens or cell remnants expressed by antigenpresenting expressed by a 09quot3 cells DC 8 macrophage Differences between MHC TCR and BCRAb function MHC I MHC II TCR BCRAb display peptide peptide no no reco nition no no peptide part Of 9 MHC native protein n binds also to binds also to alwa S receptor and special CD8 CD4 rece ytor secreted T cell kill T cell help 0 effector molecules on 3 x 2 distinct 3 x 2 distinct 3mg 3mg speCIes speCIes Single cell alleles allelic pairs unique unique variability in 30139Srggft hi0 6339322 hi0 diversity diversity single human p y p p y p gt1016 gt1x1011 genes genes generated by inheritance inheritance recombmatlo recombmatlo n Mechanism of VDJ recombination Rag1 and Rag2 proteins are B and Tlymphocyte specific components of the VDJ recombinase These molecules are only expressed in developing B and Tcells and bind to highly conserved recognition sequences flanking the gene segment Viral and certain bacterial pathogens hide inside of cells a Human immunodeficiency virus HIV the cause of AIDS CD4 Tcell lysis b Staphylococcus aureus a bacterium that colonizes human skin is the common cause of pimples and boils and can also cause food poisoning c Streptococcus pyogenes the bacterium that is the principal cause of tonsillitis and scarlet fever and can also cause ear infections e Salmonella enteritidis the bacterium that commonly causes food poisoning Salmonella infections result in two major clinical outcomes gastroenteritis and typhoid disease In both types of infections recruitment of polymorphonuclear phagocytes and macrophage apoptosis have been reported to occur in Peyer s patches However none of these responses require active proliferation of intracellular bacteria though macrophage death might promote proliferation of released bacteria that infect nearby standing cells From Peyer s patches bacteria disseminate to the reticuloendothelial system and colonise the liver and spleen These organs represent the permissive sites for Salmonella intracellular proliferation in the cases of systemic disease f epidermophyton flooccosum ringworm fungus g trypanosoma bruceiAfrican sleepy sickness hide in RBC that do not express MHC Uninfected host cells to resist new infection by virus Certain host symptoms such as aching muscles and fever are related to the production of lFNs during infection The neighboring cells in response to interferon produce large amounts of an enzyme known as protein kinase R PKR This enzyme phosphorylates a protein known as elF2 in response to new viral infections elF2 is a eukaryotic translation initiation factor that forms an inactive complex with another protein called elFZB to reduce protein synthesis within the cell Another cellular enzyme RNAse L also induced following PKR activation destroys RNA within the cells to further reduce protein synthesis of both viral and host genes Inhibited protein synthesis destroys both the virus and infected host cells Currently used in severe cases of hepatitis B and C ALARMINSDAMPs danger associated molecular patterns Recognize molecules synthesized andor released from dying eukaryotic cells ureic acid lL33 Type I lnterferons lNFa and lFNb turn on genes that shut down protein synthesis elF2 and destroy RNA RNAseL Protein kinase RPKR enzyme that phosnhorvlates a protein known as M in response to new viral infections elF2 a eukaryotic translation initiation factor that forms an inactive complex with another protein called elFZB to reduce protein synthesis within the cell Another cellular enzyme RNAse L also induced following PKR activation destroys RNA within the cells to further reduce protein synthesis of both viral and host genes Plasmacytoid dendritic cells pDCs represent one of the major sources of lFNor These cells carry patternrecognition receptors PRRs that are able to recognize evolutionarily conserved structures on infectious microorganisms as foreign and trigger an immune system reaction against them Figure l Two different types of PRRs are involved in this process TLRs Tolllike receptors and CNARs cytosolic nucleic acid receptors Located in endosomal compartments TLRs scan phagocytosed material for the presence of viral particles 1 and 1 Singlestrand RNA and double strand DNA from viral particles are recognized by TLR7 and TLR9 receptors respectively CNARs by contrast are present in all nucleated cells and allow recognition of viral particles directly at their point of entry Examples of such receptors include RIGl retinoic acidinducible gene l MDA5 melanoma differentiationassociated gene and DAl DNAdependent activator of lFNregulatory factors 1 When either of these two pathways is activated the end result is the production of type I lFNs Binding of lFNs to their respective receptors on infected cells allows the latter to activate intracellular pathways that limit pathogen replication and promote clearance Polymerizesto form a pore in target membrane Perforin l S e rine proteases which activate apoptosis Granzymes once in the cytoplasm of the target cell Granulysin I Induces apolptosis Figure 8 35 II39lquotinquoturnIiubillllugiy39I Elfes II Garland Science 2005 Proteosomea large enzyme complex with broad proteolytic activity Proteins are targeted to it by ubiquitination TAP a transporter pumping peptides from the cytoplasm to the site of the MHC l assembly in the endoplasmic reticulum Invariant chain libinds to newly synthesized MHC class II molecules in the ER and stabilizes the molecule until li is degraded and exchanged for the peptide in the endosomal compartment Antigen presentation and the Rule of Eight Antigen presenting cells APC display antigen in the context of two distinct classes of MHC molecules When antigen is presented in the context of MHC class I CTL can respond via interaction of their CD8 molecule and the MHC class I on the APC When antigen is presented in the context of MHC class II Th cell can respond via interaction of their CD4 molecule and the MHC class II on the APC CD8 x MHC class I 8 CD4 x MHC class II 8 Let s back up again for a moment and think about how the immune response originated 1 PAMPs on pathogens gt inform MF and DC of danger by an intrusion 2 Take up of pathogen via other receptors 3 protein digested into little peptides 4 peptide displayed by molecules refered to as MHC Start with explaining CD4 Tcell 1 Th1 lFNgamma macrophage against intracellular bacteria Th24 5 13 Bcell responses and antiparasite responses Th CTL lL12 Th17 promotes neutrophil inflammation VVVV 2 3 4 lllnu merel Cellmediated 7 Immunity 7 rmmunrlty Que marijth 7 quot Infraellular reeell iu39ler Phageeyrie eed 5 New Ii33935 microbes microbes in E E39QWFUSESJI Responding I lymphmytes Helper quot Bytefxie B lymphocyte T lymphocyte T lymphocyte Secreted a 39 i1 antibody I Effecter 1939 meelhanl em El k Activred 5 Killed infected cell quot0639 infeetiene erudl macrophage Kill infected cells Functions eliminate Eliininaep Bedfelimieee extracellular phageeyteeed F39ESEI VDIII S microbes miereibee ef infeetien bbae er al Basic immunology 4e Copyright 39339 2014 2011 ZEUB ZUIDVE 2064 2001 by Saunders an imp39rinrlf of lElISE U39lET 1m Adjuvant a substance distinct from the antigen or a pathogens that promotes the accumulation and activation of antigenpresenting cells at the site of antigen exposure It acts as the danger signal that TLRs promote T cell specific for Cytokinee liLu lU and self antigen becomes TGFB produced by a regulatory T cell Tmg inhibit other ng selfnreactiv e T cells The isotype of an antibody is determined by its constant region Bcells can change their isotype in an ordered sequence during an immune response but not their specificity Isotypes can switch orderly from IgM to IgG to IgA and finally to IgE This does not change the soecificitv of the antibody but it effects its function including its biological distribution its interaction with complement and its binding to different Fc receptors Thus antibodies have two biologically critical regions The specific antigen recognition site and the Fcregion of their isotype shared with different specific antibodies
Are you sure you want to buy this material for
You're already Subscribed!
Looks like you've already subscribed to StudySoup, you won't need to purchase another subscription to get this material. To access this material simply click 'View Full Document'