Microbiology 2500A/B Immunology summary.docx

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Department
Microbiology and Immunology
Course
Microbiology and Immunology 2500A/B
Professor
John Mc Cormick
Semester
Fall

Description
INNATE IMMUNITY WBCs (leukocytes) → phagocytes + lymphocytes Soluble molecules secreted by an activated cell: cytokines (innate & adaptive, secreted by all ACTIVATED CELLS, dictate what stem cell becomes), acute phase p-, complement p-, antibodies (all in plasma) Myeloid progenitor → phagocyte (e.g. neutrophil). Lymphoid progenitor → lymphocytes 4 Types of PRRs on Innate Cells Location C-type lectin receptors cell surface Toll-like receptors cell surface + endosomes RIG-I-like receptors cytoplasm NOD-like receptors cytoplasm CTRN = Come To Rachel’s Now PAMP → low mutation rate Innate cell Location Pathogen Mechanism killed Neutrophil (very short Blood Extracellular Phagocytosis lived) bacteria *Macrophage {large} Tissue Extracellular Phagocytosis (*from blood monocyte) bacteria Call adaptive *Dendritic Cell Blood, Extracellular Phagocytosis Immature: phagocyte lymph & Mature: adaptive cell tissue NK Cells (lymphocyte) Blood Intracellular Apoptosis of Has toxic enzymes (viral infectioninfected cell NK cells kill virus infected cells before T cells start Enzymes in lysosome: defensins, lysozyme (cell wall), NADPH oxidase (respiratory burst), nitric oxide synthetase Cytokine Families: o Chemokines attract immune cells o Interferon (IFN) – II, III o Type I (alpha & beta) released by virus infected cells (and cancer cells) attract NK & induce uninfected cells to produce antiviral enzymes (block viral replication). All cells have IFN receptors o Tumor Necrosis Factor (TNF). o Interleukins (IL) TNF, IL-1 and 6 (vasodilation), chemokines released b/c phagocyte got activated by PAMP. Some cytokines in blood. These 3 cytokines also activate hypothalamus → prostaglandins → fever to kill pathogen. These 3 cytokines also activate hepatocytes to secrete acute phase p- and complement p- (9C, always get C3B activated and bind to pathogen) APP and CP (in circulation, enter infected tissue) help “attach” extracellular pathogens to phagocytes. Binds to pathogen and phagocyte (via APPR or CPR). APP & CP enhance phagocytosis by increasing the uptake of pathogens by phagocytes 3 receptors on phagocyte that bind extracellular pathogens: PRRs (1 ), acute-phase p- receptor, complement p- receptor CP cause vasodilation, along with TNF, IL-1, IL-6 cytokines → VASODILATION Viral infection? Need monocytes, neutrophils, immature DCs (to kill extracelluar virus) AS WELL AS NK cells (intracellular virus) {Cell-mediated adaptive immunity is the major immune response against intracellular bacteria} HUMORAL ADAPTIVE IMMUNITY (5-10 days)  B lymphocytes in HUMORAL immunity. T lymphocytes in CELL-MEDIATED immunity  When B cell Igs bind an extracellular pathogen, it becomes a plasma cell and which sheds Ig as antibodies  Each B cell expresses many IDENTICAL copies of a UNIQUE immunoglobulin molecule (variable region)  Each B cell has a variable region specific for one unique epitope on an antigen. 1 antigen, different epitopes  A B cell that binds an antigen undergoes mitosis = CLONAL EXPANSION  Antibody function is defined by what the constant region binds to  Neutralization: antibody coats pathogen, prevents pathogen entry into cells (e.g. virus)  Opsonization: antibody coats pathogen, constant region binds to Fc receptor (FcR) on phagocyte → phagocytosis  Activation of complement p-: Ab coats pathogen, constant region binds complement protein, activates complement → C3b formation → complement mediated phagocytosis (b/c of comp. receptors on phagocyte)  5 classes of Ig molecules/Ab = ISOTYPES. Differences in constant heavy chain (length, hinge)  When the B cell arrives in circulation as a naïve B cell, it is co-expressing IgM (first antibody every time, always produced with every exposure) and IgD (not secreted!!); 2 isotypes  IgG: most abundant antibody in blood, provides PASSIVE IMMUNITY to newborn (maternal IgG is only isotype capable of crossing the placenta). IgG has a hinge, is more effective than IgM  IgA is highest levels in the MALT tissues. Most abundant antibody in any bodily secretions (breast milk → passive immunity). Has a hinge, therefore better than IgM  IgE instrumental in anti-parasitic humoral immunity andinvolved in allergic reactions  Antibodies for extracellular bacteria/virus: IgG, IgM, IgA  If circulating naïve B cell binds an antigen in lymph node (it may also bind a T cell), it undergoes clonal expansion, differentiates into a plasma cell and secretes antibodies (returns to infected tissue)  T-independent (TI) response against non-protein antigens (polysaccharides, lipid). Pathogen activates B cell to become a plasma cell to secrete antibodies (IgM, IgD). Produces short-lived plasma cells, secrete mainly IgM Abs, do not produce memory B cells  T-dependent (TD) response against protein antigens (B cell activated by pathogen & T cell). When this binding interaction occurs, the T cell becomes activated and will begin to secrete cytokines on to the B cell. So the B cell needs to bind pathogen and a T cell before it becomes a plasma cell
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