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Immuno Lec 1

Commensals Normal Flora, microbes that coexist with humans without causing disease. Non pathogenic
Pathogens Microbes capable of causing human disease, can attain 3 states of growth in the human body.
Colonization Establishment of proliferating microbes on skin.
Infection The proliferation of microbes in the tissues along with induction of the immune system. The numbers have reached a threshold level
Disease Proliferation of microbes in tissues, immune response and resulting damage or impairment of body functions
Once Infection Occurs, what pathways can microorganisms follow Becoming commensals, elimination, carrier state, or pathogenicity.
Three main levels of microbial threat response Barriers, Innate immunity, Adaptive Immunity
Innate Immunity non specific. 0-96 hours. Phagocytosis, complement, inflammation, cytokine release, NK cell killing
Adaptive Immunity Specific, greater than 96 hours. Humoral - B cells and Antibodies Cell Mediated - T cells and cytokines
Barriers to infection Respiratory Tract, Skin, GI Tract, Urogenital Tract.
Defense Mechanisms of the Skin Sloughing of keratinocytes, fatty acids(lower pH), A-Defensins B-Defensins Cathelecidins, lysozyme, Rnase and Dnase.
A and B Defensins and Cathelecidins Penetrate the bacterial cell wall, disrupt, ultimately make it die.
Lysozyme Degrade Peptidoglycan which is main component of bacterial cell wall.
Components of Innate Immunity Macrophages, Granulocytes, NK cells, Complement, and other chemicals (Hcl, lysozyme)
Characteristics of Innate Immunity Immediate, Non Specific, Response is not enhanced on repeated exposure to pathogen.
Why can't you have adaptive immunity without innate immunity? There is an interplay. Innate generates mediators required to activate the adaptive immune response.
Cell Lineage Start at Hematopoeitic Stem Cell. This becomes Myeloid Lineage of Lymphoid Lineage.
Myeloid Lineage Thrombocytic(thrombocytes), erthyrocytic(erythrocytes), granulocytic(eosinophils, basophils, neutrophils), monocytic(macrophages, monocytes, dendritic cells).
Lymphoid lineage Dendritic Cells, NK cells, T cells, B cells
Macrophages Phagocytic. Located in tissues. longer lifecycle than neutrophil. APC. Secrete cytokines to draw additional macrophages into areas to fight infection and that help activate T and B cells.
Neutrophils Phagocytic. Short life cycle. Located in blood. LowGranular release of antibacterial compounds. Does not engulf, destroys membrane without having to engulf. Not an APC.
Pattern Recognition Receptors Present on phagocytes. They recognize patterns on microbes, not specific features. Innate Immunity. Generally they recognize PAMP.
Pathogen Associated Molecular Patterns PRR's bind to this. These are located on pathogens. They are not specific. Includes the Toll Like Receptors.
Phagocytosis The PRR engages a PAMP. It then encloses the pathogen in a clathrin coated pit. Now it is a phagosome. It fuses with a lysosome. Now it is a phagolysosome.
Macropinocytosis Not receptor mediated. Non specific. Cell extends out processes, engulfs fluids and any microbes present in extracellular environment. becomes cytoplasmic vesicle, then a phagolysosome.
What occurs after a phagolysosome is formed Oxidative Burst and oxygen independent pathway.
Oxidative Burst Key enzyme is NADPH Oxidase. Turns O2 into a superoxide (O2 radical). Then, superoxide dismutase turns that into H2O2. Then, myelo peroxidase turns that into a hydroxyl radical or a hypoclhlorite radical. These physically rupture the membrane.
Oxygen independent Pathway after phagolysosome is formed Cell can produce proteases that destroy the pathogen.
Complement System Innate and Acquired Immunity. Important for destroying bacterial pathogens. 20 or more proteins in serum. Can cause lysis, enhance phagocytosis and participate in inflammation.
Three methods of activation of complement Bacterial Surface. Acute phase protein. Antibody. First two are Innate. Antibody is Adaptive.
How does complement enhance phagocytosis? It is also called opsinization. Complement components can coat bacteria, make more attractive to phagocytic cells. Phagocytic cells have receptor for complement.
How does lysis occur in complement? 20 serum proteins are circulating, already made. bacterial surface is sticky to complement. they bind, initiate complement, and then lysis occurs.
How do acute phase proteins activate complement? They bind to pathogen and initiate cascade.
Four hallmarks of Inflammation Rubor, Calor, Dolor, Tumor. Rumor - redness. Calor - Warmth. dolor - Pain tumor - Swelling
Three main effects of inflammation increase blood flow to dilute toxic agents increase capillary permeability to facilitate transmission of large molecules across endothelium increased migration of cells into tissues to destroy bacteria, remove debris, and restore normal tissue structure
Six steps of inflammation Tissue Injury, Vasodilation, Increased Permeability, Emigration of leukocytes, chemotaxis, phagocytosis.
Early Inflammatory Mediators Histamine
Histamine Made in mast cells. Increase vascular permeability
Late Inflammatory Mediators Cytokines, released by activated macrophages. IL-1, TNF-a, IL-8, IL-12
Interleukin-1 Fever, induction of adhesion proteins and acute phase proteins
Tumor Necrosis Factor alpha Fever, chemotactic
Importance of adhesion proteins important for margination. in order to undergo diapedesis, they must emigrate.
Interleukin-8 Chemotactic for neutrophils
Interleukin-12 Activates NK Cells
Two phases of Inflammation Acute, 0-72 hrs Chronic - 72+ Hrs
Acute Inflammation 0-72 hrs. Sequential recruitment of cells, first neutrophils (principal inflammatory cell), then monocytes/macrophages, then lymphocytes.
Chronic inflammation Long Term. When causitive agents not destroyed. Formation of granulomas. To isolate or confine the inflammatory agent. Influx of macrophages, they form giant cells. Becomes encased in T lymphocytes, some B.
Fever Elevated Body Temperature Produced by pyrogens. Il-1, Il-6, TNFa
Interferons Proteins synthesized by many cell types in response to viral infection IFNa, IFNb. Also activate NK cells. They can degrade viral nucleic acids.
Natural Killer Cells Innate Immune response. Viral infection. Generalized. Recognizes KAR and KIR. If the NK cell can only bind its KAR and not its KIR, then the NK cell destroys it by releasing granular contents.
KAR Killer Activation Receptor. When infected or under stress, cells show MICa and MICb, stress molecules. KAR binds to this.
KIR Killer Inhibition Receptor. This binds to MHC1 on a cell surface. If this binds to MHC1, then it will not engage.
Why do viruses downregulate MHC1 They do this to avoid Cytotoxic T cells because MHC1 holds out cellular contents.
Primary Immunodeficiency Genetic Defect
Secondary Immunodeficiency Secondary to viral infection. Decreased function. Ie. HIV.
Neutropenia Decreased numbers in immunodeficiency
Chronic Granulomatous disease X linked recessive - cytochrome B Autosomal recessive - NADPH Oxidase. no production of superoxide radicals. Cells can get to pathogen, engulf it, can't destroy it. formation of granulomas. Usually opportunistic microbes. Treated with gamma interferon.
Why is gamma interferon used for CGD It activates macrophages, and boosts the oxygen independent pathway.
Why does CGD only affect catalase positive individuals? Because Catalase degrades H2O2. H2O2 is the final step in production of the hydroxyl radical and hypochlorite. If you are catalase negative, you can use H2O2 to break down. If you are catalase positive, you break it down yourself.
Leukocytes Adhesion Deficiency CD18. Autosomal Recessive. CD18 (B-integrin) required for phagocytic adhesion and migration across vessel walls. encapsulated bacteria
Chediak Higashi Syndrome LYST - defect in vesical fusion with macrophage. reduced killing ability. exclusively macrophages. LYST - lysosomal transport.
Pathogens of Adaptive Immune System Extracellular (HUMORAL) - bacteria, toxins, parasites, fungi Intracellular (Cell Mediated) - viruses, parasites, bacteria.
B cells vs T cells in the recognition of Antigens B cells - NATIVE. T cells - PROCESSED.
Primary Immune Response First time you see the pathogen. You won't see any Abs in blood until day 4-5. days 1-5, Innate system is working. First Ab at day 5 is IgM, then IgG. Not Strong. weak affinity.
Secondary Immune Response Lag phase is gone. This is upon repeated exposure. IgG occurs almost immediately due to the abundant memory cells. Also, sustained much longer. Faster and more effective.
postulates of clonal selection hypothesis 1.Unique Specificity of Lymphocyte Receptor 2. binding with high affinity leads to lymphocyte activation 3. memory B cells formed will have identical specificity 4. Self recognizing lymphocytes destroyed.
Created by: nady