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by: Winona McClure

Immunology MIP 342

Winona McClure
GPA 3.71

Alan Schenkel

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Alan Schenkel
Class Notes
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This 22 page Class Notes was uploaded by Winona McClure on Tuesday September 22, 2015. The Class Notes belongs to MIP 342 at Colorado State University taught by Alan Schenkel in Fall. Since its upload, it has received 44 views. For similar materials see /class/210241/mip-342-colorado-state-university in Microbiology at Colorado State University.

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Date Created: 09/22/15
30 January What do I need to know Innate Immune System Receptors How do the cells and molecules of the innate response recognize and attack broad classes of pathogens How do llwhite blood cells get to tissues to attack pathogens Cytokines and chemokines compare and contrast Innate immunity specificity inherited in the genome expressed by all cells of a particular type triggers immediate response recognizes broad classes of pathogens interacts with a range of molecular structures of a given type Adaptive immunity encoded in multiple gene segments requires gene rearrangement clonal distribution able to discriminate between even closely related molecular structures Functional Consequences of Signaling Cell growth Proliferation Mitogens cause mitosissuperantigens 9 vigorous nonspecific growth Death Function Movement to different tissues Bone marrow to thymus or peripheral tissues for development Movement to inflamed tissueslocal lymphoid tissues extravasation MacrophagesDCs endocytosis ofantigens 9 cytokines antigen presentation killing of endosomal pathogens 9 migration to local LNs T cells NK cellsy6 cells 9 cytokines activate killing 9 inhibition of immune response 03 B cells 9 antibody secretion Development of memory in B and T cells How does a cell signal another cell Concept of quotreceptorquot and quotligandquot Direct interaction APC antigenpresenting cell eg dendritic cell and T cell Cytokineschemokines quotindirectquot Autocrine self Paracrine local cells Endocrine through body Cytosolic and nuclear targets Cross talk and feed back loops quotSecond messengers proteins and small molecules Phosphorylation Calcium Phosphoinositolsprostaglandinsterols Cells of the Innate Response Neutrophils Monocytes 9 macrophagesDCs Natural killer lymphocytes hunt quotstrangequot cells infected Gamma delta y6 T cells recognize lipids and other signals not very motile Invariant NKT cells recognize lipids and other signals Blmarginal zone B cells act like macrophages quotMarginal zone in spleen Use antibody molecules to ingest things Innatelike lymphocytes Bl cells make natural antibody protect against infection ligands not MHC associated cannot be boosted found in non lymphoid tissues unlike quotconventionalquot 32 B cells peritoneal cavity spleen Epithelial y6 cells produce cytokines rapidly ligands are MHC class IB associated most line epithelium some in blood NK T cells produce cytokines rapidly ligands are lipids bound to CDld y6 and NK good at recognizing lipids Bl cell binds bacterial capsular polysaccharide or cellwall components and receives a signal IL5 from accessory cells 9 31 cell secretes IgM antipolysaccharide antibody 9 IgM binds polysaccharide capsule 9 activation of complement and removal of bacteria Natural antibody low amounts of lots of kinds of antibodies Cell can spontaneously activate itself Detection of pathogens by the innate immune response receptors and chemotaxis Macrophages dendritic cells and neutrophils have phagocytic receptors that bind microbes and their components Sugar receptors recognize repeated sugar structures Scavenger receptors recognize a lot doublestranded RNA lipopolysaccharides misfolded proteins ampc Respiratory or oxidative burst Neutrophils engulf and kill the microbes to which they bind 9 bacterial fMet LeuPhe peptides activate RacZ and bacteria are taken up into phagosomes 9 phagosomes fuse with primary and secondary granules RacZ induces assembly of a functional NADPH oxidase in the 39 U 39 39 leading to g 39 of 02 Acidification as a result of ion influx releases granule proteases from granule matrix Digestive enzymes free radicals digest Bits remain macrophage or neutrophil shows to T cells Kill bacteria via acidification change pH toxic oxygenderived products toxic nitrogen oxides antimicrobial peptides enzymes starving Cytokines LlB interleukin Activates vascular endothelium activates lymphocytes local tissue destruction increases access of effector cells Fever production of L6 TNFot tumor necrosis factor Activates vascular endothelium and increases vascular permeability which leads to increased entry of IgG complement and cells to tissues and increased fluid drainage to lymph nodes Fever mobilization of metabolites shock L6 Lymphocyte activation increased antibody production Fever induces acutephase protein production antibody production L12 Activates NK cells induces the differentiation of CD4 T cells into THl cells IFNs interferons Activates NK cells induces the differentiation of CD4 cells into THl cells Chemokine CXCLS Chemotactic factor recruits neutrophils basophils and T cells to site of infection Directs traffic to signaling macrophage Chemotaxis Bacteria induce macrophages to produce L6 which acts on hepatocytes to induce synthesis of acute phase proteins 9 C reactive protein binds phosphochoine on bacterial surfaces acting as an opsonin and also activating complement mannosebinding ectin binds mannose residues on bacterial surfaces acting as an opsonin and also activating complement SPA SPD also activate complement fibrinogen clots blood LlBlL6TNFot Liver acutephase proteins Creactive protein mannosebinding ectin 9 activation of complement opsonization Bone marrow 9 r C Hypothalamus increased body temperature 9 decreased viral and bacterial replication increased antigen processing increased specific immune response Fat muscle protein and energy mobilization to allow increased body temperature 9 decreased viral and bacterial replication increased antigen processing increased specific immune response Dendritic cells TNFot stimulates migration to lymph nodes and maturation 9 initiation of adaptive immune response GPCR G protein coupled receptor Before ligand binding a GPCR is not associated with a G protein inactive G protein has GDP bound 9 ligand binding causes a conformational change in the receptor which enables it to associate with the G protein G protein releases GDP and binds GTP 9 G protein dissociates into 01 and yB subunits both of which can activate other proteins activation of the GTPases Rac Rho and CDC42 stimulates chemotaxis or the respiratory burst 9 the ot subunit cleaves GTP to GDP allowing the 01 and yB subunits to reassociate signaling terminates 7 transmembrane loops Receptors on side of cell chemokine comes from activated cell moves in that direction Cytokines produced by macrophages cause dilation of local small blood vessels 9 leukocytes move to periphery of blood vessel as a result of increased expression of adhesion molecules by endothelium 9 leukocytes extravasate at site of infection 9 blood clotting occurs in the microvessels keeps infection from spreading Sepsis inflammation gone wrong Local infection with Gramnegative bacteria Macrophages activated to secrete TNFot in the tissue 9 increased release of plasma proteins into tissue Increase phagocyte and lymphocyte migration into tissue Increased platelet adhesion to blood vessel wall 9 phagocytosis of bacteria Local vessel occlusion Plasma and cells drain to local lymph nodes 9 removal of infection adapative immunity Systemic infection with Gramnegative bacteria sepsis Macrophages activated in the liver and spleen secrete TNFot into the bloodstream 9 systemic edema causing decreased blood volume hypoproteinemia and neutropenia followed by neutrophilia Decreased blood volume causes collapse of vessels 9 Disseminated intravascular coagulation leading to wasting and multiple organ failure 9 death 28 January Lag phase between exposure and response 7 10 days B cells make antibodiesBCR T cells use the TCR conserved structures for antigen recognition B cells have B cell receptor antibody attached to cell membrane Variable region antigenbinding site Constant region effector function Specific antibody bacterial toxins 9 forms antigenantibody complex neutralization 9 macrophage recognizes antigenantibody complex ingestion Specific antibody bacteria in extracellular space 9 opsonization 9 ingestion by macrophage Specific antibody bacteria in plasma 9 complement activation 9 lysis and ingestion The epitopes recognized by Tcell receptors are often buried 9 the antigen must first be broken down into peptide fragments 9 the epitope peptide binds to a self molecule an MHC molecule 9 the T cell receptor binds to a complex of MHC molecule and epitope peptide Antigen Presentation of viral or bacterial peptides on Major Histocompatibility Complex molecules M HC All cells have MHC in case of viral or intracellular infection Recognized by CD8 cytotoxic cells Only immune cells have MHC II to communicate to CD4 helper T cells what they found and I U are D 39 Ithis way The immune system protects against four classes of pathogens Extracellular bacteria parasites fungi Streptococcus pneumonia causes pneumonia Clostridium tetani causes tetanus Trypanosomabrucei causes sleeping sickness Pneumocystis carinii causes Pneumocystis pneumonia Intracellular bacteria parasites Mycobacterium Ieprae causes leprosy Leishmaniadonovani causes leishmaniasis Plasmodium falciparum causes malaria Viruses intracellular Variola causes smallpox Influenza causes flu Varicella causes chickenpox Parasitic worms extracellular Ascaris causes ascariasis Schistosoma causes schistosom iasis Cytotoxic T cell recognizes complex of viral peptide with MHC class I and kills infected cell MHC Class loading of peptides Virus infects cells 9 viral proteins synthesized in cytosol 9 peptide fragments of viral proteins by MHC class I in ER 9 bound peptides transported by MHC class I to the cell surface MHC Class II recognition by CD4 T helper cells THl cell recognizes complex of bacterial peptide with MHC class II and activates macrophage Helper T cell recognizes complex of antigenic peptide with MHC class II and activates B cell Antigenreceptor binding and costimulation of T cell by dendritic cell 9 proliferation and differentiation of T cell to acquire effector function Antigenreceptor binding and activation of B cell by T cell 9 proliferation and differentiation of B cell to acquire effector function Secondary Immune Response A pathogen that attacked or is in a vaccine before attacks again Antibody is already there from the first time Memory B and T cells from the first time see the antigens again and proliferate rapidly Attack is usually quickly rejected Organs of the Immune System Primary lymphoid organs Thymus where T cells are quoteducatedquot Bone marrow Bursa of Fabricius avian where B cells are educatedquot Secondary lymphoid organs Lymph nodes Spleen T cells and B cells may be activated here Tertiary lymphoid organs Gutassociated lymphoid tissue GALT Mucosalassociated lymphoid tissue MALT Skinassociated lymphoid tissue SALT Lymphatic System Blood plasma leaks from capillaries Interstitial fluid lymph Lymphatic capillaries Afferent lymphatic vessels Lymph node Efferent lymphatic vessels Lymphatic trunks Thoracic duct Vena cava Thymus education site for T cells Right below capsule cortex Baby T cells thymocytes Must pass through network of dendritic and medullary epithelial or stromal cells Have MHC molecules if one activates T cell is killed off recognized self Primary Lymphoid Organs for Bcell Maturation Bursa of Fabricius in avian species Bone marrow is site of Bcell maturation in mammals quotBursal equivalent lealPeyer s patches in lambs and calves Lymph node Follicles Contain germinal centers primarily B cell zones paracortical area mostly T cells If B cell recognizes something proliferates germinal center grows Afterwards becomes senescent remembers antigen High endothelial venules allow naive T and B cells to enter lymph node If activated B cells stay T cells drain through efferent lymphatics Spleen in a Secondary Lymphoid Organ Primary job get rid of deaddying red blood cells Lifespan 60 days Dying red blood cells eaten by macrophages in red pulp PALS and germinal centers make up white pulp Tonsils are MucosaAssociated Lymphoid Tissue MALT Protect sinuses in back of throat Adenoids dump antibody into sinuses of nasal cavity Peyer s patches are covered by an epithelial layer containing specialized cells called M cells which have characteristic membrane ruffles M cells bring in things from intestine Processed by dendritic cells germinal centers follicles SkinAssociated Lymphoid Tissue SALT Langerhans cells dendritic cells Anything that touches is eaten Taken to lymph nodes Dendritic Cells Initiate Adaptive Immune Responses Immature dendritic cells reside in peripheral tissues 9 dendritic cells migrate via afferent lymphatics to regional lymph nodes 9 mature dendritic cell in the deep cortex 23 January Course Overview Where are we going Chapter 1 Overview of the whole course very useful but detailed Dr Schenkel Building blocks of Immunology and nomenclature Chapters 2 7 Complement Dr ZabelDr Michel How does the innate immune system work The adaptive response how specific immune responses are made Cell signaling Dr Taylor The Functional Immune Response Chapter 8 How B and T progenitor cells are educated to become nai39ve but functional B and T cells Chapters 9 10 Activation and function ofT and B cells Chapter 11 The response to infection Chapter 12 Mucosal immunity Dr Zabel and Dr Schenkel The Dysfunctional Immune Response Chapter 13 Pathogen evasion of the response to infection immunodeficiencies Chapter 16 Tumor Immunology and Vaccines Chapter 14 Allergy and Hypersensitivities Immune overreaction Chapter 15 Tolerance and Transplantation Synthesis from past courses ChemistryPhysics Molecular interactions Hydrophobicity Eukaryotic Cell biology Cell Division Cell signaling Genetics Transcription and translation Chapter 1 What I want you to know Cells of the immune system names basic function Organs of the immune system organization That there is a lot of confusing stuff in chapter 1 that will make sense later Basic immunological terms Mbody erators ANTIGENS Ag are substances recognized by ANTIBODIES Immunoglobulin Ig Ab and T LYMPHOCYTES T CELLS Antibodies are made by B LYMPHOCYTES B CELLS T cells help B cells make antibodies T HELPER Th cells CD4 T cells T cells kill infected cells T CYTOTOXIC CTL CD8 T cells Epitope is recognized region on antigen Antigen can have multiple epitopes Barriers Barriers to invasion and infection skin and mucous membranes Rapidly regenerating surfaces peristaltic movement mucociliary escalator vomiting flow of urinetears coughing Innate immunity cellular and humoral defenses Lysosyme sebaceousmucous secretions stomach acid commensal organisms complement proteins phagocytosis NK cells Adaptive immunity cellular and humoral defenses Antibodies B cells cytokines T helper cells cytotoxic T cells Humoral Responses Proteins in liquid The humoral responses are basically llnot cells eg complement antibodies defensins small antibacterial proteins Where did the name come from From the ancient Greek Four Humors Thought to control health and emotions Blood Sanguine thought to come from liver which is true for complement Reason George Washington was bled to death Yellow Bile Choleric from spleen Phlegm Phlegmatic from lung Black bile Melancholic gall bladder 25 January Innate immune response Recognizes broad classes of antigens lnbuilt immunity to resist infection Present from birth Not antigenspecific Not enhanced by second exposure Has no memory Uses cellular and humoral components s poorly effective without adaptive immunity Also involved in the triggering and amplification of adaptive immune responses Adaptive immunity Immunity established to adapt to infection Learned by experience Confers pathogenspecific immunity Enhanced by second exposure Has memory Uses cellular and humoral components s poorly effective without innate immunity Antibodies reflect infections to which an individual has been exposed diagnostic for infection llBuffy coat or leukocytes white blood cells Red blood cells are dense full of iron Plasma where antibodies complement and other quothumoralquot components are found Serum is liquid from clotted blood Phil affinity for certain dyes Basophil basic stains lt1 of white blood cells Neutrophil neither base nor eosin 24 hour lifespan 50 70 Eosinophil eosin stain 1 3 All of these have multilobed nuclei Lymphocyte B cell T cell or natural killer cells Activated have round nucleus Monocyte bean shaped nucleus large cell All white blood cells come from bone marrow Erythroblast produces red blood cells Common lymphoid progenitor gives rise to T cell B cell NK cell Mega karyocyte platelets Monocyte differentiates into Macrophage Phagocytosis and activation of bactericidal mechanisms Antigen presentation Can fuse to each other become giant cell Dendritic cell Antigen uptake in peripheral sites Antigen presentation in lymph nodes Very mobile Macrophages and dendritic cells express receptors for many microbial constituents Allow to recognize microbial surfaces Scavenger receptor grabs lots of things Neutrophil First responder Explode themselves spray bleachperoxide Phagocytosis and activation of bactericidal mechanisms Eosinophil Allergies parasites Killing of antibodycoated parasites Eosinophilsbasophils also present antigens Basophil Promotion of allergic responses and augmentation of antiparasitic immunity Mast cell Release of granules containing histamine and other active agents Small lymphocyte quiescent not yet functional not activated Lack of cytoplasm ER Activated 9 becomes lymphoblast Differentiates into effector T cells or effector B cells Effector B cells plasma cells Great amounts of cytoplasm B cell makes antibody CD4 T cell directs response onoff CD8 T cell kills infected cells Natural killer NK cell Releases lytic granules that kill some virusinfected cells Phases of the immune response Response Typical time after infection to start of response Duration of response Inflammation complement activation phagocytosis and destruction of pathogen Innate immune response Minutes Days Interaction between antigenpresenting dendritic cells and antigenspecific T cells recognition of antigen adhesion co stimulation Tcell proliferation and differentiation Hours Days Activation of antigen Adaptive immune specific B cells Hours Days response Formation of effector and memory T cells Days Weeks Interaction of T cells with B cells formation of germinal centers Formation of effector B cells plasma cells and memory B cells Production of antibody Days Weeks Emigration of effector lymphocytes from A few days Weeks peripheral lymphoid organs Effector cells and antibodies eliminate the A few days Weeks pathogen Immunological memory Maintenance of memory B cells and T cells and high serum or mucosal antibody levels Protection against reinfection Days to weeks Can be lifelong Infection The beginning of the immune response Bacteria eaten by macrophage Bacteria trigger macrophages to release cytokines and chemokines Vasodilation and increased vascular permeability cause redness heat and swelling Inflammatory cells migrate into tissue releasing inflammatory mediators that cause pain Primary Immune Response Macrophages natural killers y6 gamma delta T cells sound the red alert cytokines and chemokines if infection is detected Neutrophils and monocytes will respond within minutes and hours Monocytes will turn into macrophages and dendritic cells DCs DCs will carry antigens to nearby LNs lymph nodes DCs will show antigens to B and T cells 1 in 100000 lymphocytes will recognize a specific epitope and proliferate clonal expansion B cells will begin to make antibody with CD4 T cell help CD4 and CD8 T cells will migrate across body to site of wound and beyond to kill infected cells Human Lymphoid System Upper right quadrant drains through right lymphatic vein to right subclavian vein Everything else drains to thoracic duct to left subclavian vein Lymphatics Nonmuscularized lymphatics drain to LNs then to large collecting lymphatics Prenodal have muscle APCs antigenpresenting cells in wall Collecting lymphatics are muscular and have a lumenvascularized Lower order animals nonvertebrates fish have lymphatic hearts to pump lymph fluid Mammals use valves to help push fluid forward like vascular veins regulated by eNOS Lymphocyte Recirculation Blood 9 tissues 9 lymph 9 blood Completes cycle 1 2 timesday Activated B cells remain in lymph nodes Activated T cells travel all over Afferent lymphatics 9 lymph nodes 9 efferent lymphatics A comes before E Primary Immune Response B cells will make better antibodies Eventually the war is won or lost Assuming the immune response wins which it does gt99 of the time several things happen Generation of memory Most B and T cells will die but a few will remain and live Wound healing Macrophages and T cells coordinate the end of the response Postulates of the clonal selection hypothesis Each lymphocyte bears a single type of receptor with a unique specificity Interaction between a foreign molecule and a lymphocyte receptor capable of binding that molecule with high affinity leads to lymphocyte activation The differentiated effector cells derived from an activated lymphocyte will bear receptors of identical specificity to those of the parental cell from which that lymphocyte was derived Lymphocytes bearing receptors specific for ubiquitous self molecules are deleted at an early staged in lymphoid cell development and are therefore absent from the repertoire of mature lymphocytes Inherited gene segments 9 unique combination of segments becomes joined by somatic gene rearrangement 9 chains pain to give a unique receptor for each lymphocyte A single progenitor cell gives rise to a large number of lymphocytes each with a different specificity 9 removal of potentially selfreactive immature lymphocytes by clonal deletion 9 pool of mature nai39ve 39 r39 9 r quot39 39 and quotquot 39 39 ofactivated specific lymphocytes to form a clone of effector cells effector cells eliminate antigen


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