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UM BIOM 250N - Immunological Memory and Adaptive Immunity
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BIOM 250n 1st Edition Lecture 20Outline of Last Lecture I. Classes of T cellsII. Antigen-Presenting CellsIII. The Cellular ResponseOutline of Current Lecture I. Cytotoxic T cellsII. Extracellular Killer CellsIII. ADCCIV. CytokinesV. Immunological MemoryVI. Types of Adaptive ImmunityCurrent LectureI. Cytotoxic T cellsa. These can also be stimulated by correct epitope in MHC from an infected or diseased self-cellb. Remember, an infected or diseased cell will have foreign epitopes in its MHCc. Activation by this MHC causes T cell to produce:i. Perforins that form pores in target cellii. Granzymes that indude apoptosisII. Extracellular Killer Cellsa. Kill pathogen infected or tumor cellsi. Can also attack large pathogensb. Natural killer cells i. Innate cells; do not need antigen stimulationii. Checks MHC on infected self-cellsiii. If missing, kills cell with perforinc. Cytotoxic T lymphocytesThese notes represent a detailed interpretation of the professor’s lecture. GradeBuddy is best used as a supplement to your own notes, not as a substitute.i. Activated by antigen in MHC ii. Can recognize pathogen coated with antibodyd. Activated macrophagesi. Can also recognize pathogen coated with antibodyIII. Antibody-dependent cell-mediated cytotoxicity (ADCC)a. Occurs if the pathogen is too large for phagocytosisb. First—target coated with antibodiesc. Attacking immune cells bind to antibody with Fc receptord. Attacking cells secrete components that can lyse the target membraneIV. Cytokinesa. Signaling proteins or glycoproteinsi. Produced by immune cellsii. Interact only with cells that have the specific receptors for the released cytokineb. Many different cytokines—but what you need to know for this class is:i. Interleukins—induce inflammationii. Interferons—protect against viral infectioniii. Tumor necrosis factor—induces inflammatory reactions; can be involved in autoimmune diseasesV. Immunological Memorya. Starts with production of antibody following first contact with antigeni. First IgM is made; 7-10 days to peak antibody titerii. Next, IgG is made; 10-14 days to peakiii. As infection resolved antibody titer dropsiv. Titer: concentration or amount of antibody in bloodb. Secondary response or memory responsei. Next exposure to antigen causes fast antibody response; 2-7 days to peak titerii. Antibody titer is much higher during secondary responseiii. This is due to memory cells quickly changing to plasma cells, pumping outthe antibodyVI. Types of Adaptive Immunitya. Naturally acquired active immunityi. Develops from illness and recoveryii. Can be lifelong or short termb. Naturally acquired passive immunityi. Transfer of antibodies from mother to infantii. Can be transplacental or through first milk (colostrum)iii. Immunity lasts only a few weeks to monthsc. Artificially acquired active immunityi. Provided by vaccination, injection of antigen into the bodyd. Artificially acquired passive immunityi. Injection of antibody into patientii. Antibodies derived from animal or person previously exposed to diseasee. Terminology:i. Antiserum: term for serum containing antibodiesii. Immunoglobulins: antibodiesiii. Gamma globulin: serum fraction containing the most antibody1. Antibody protection is


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UM BIOM 250N - Immunological Memory and Adaptive Immunity

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