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HAN 202 Immune
Immune System
| Question | Answer |
|---|---|
| pathogen | agents of disease, includes viruses, bacteria, fungi, other microbes |
| microbiome | microorganisms that reside on and in the human body |
| innate immunity | defenses we are born with, local effects, nonspecific, lacks memory |
| external barriers | first line of defense, skin and mucous membranes |
| protective features of skin | tough, dry, sheds dead keratinocytes, acid mantle inhibits bacterial growth, skin peptides kill microbes |
| protective features of mucous membranes | traps microbes, lusozymes destroy beacterial cell walls |
| phagocytes | cells that engulf foreign matter |
| neutrophils | wbcs, wander in connective tissue killing bacteria, use neutrophil extracellular trap to ensnare bacteria |
| monocytes | wbcs, travel from blood to connective tissue, transforms into macrophages |
| margination | wbcs move away towards inner lining of blood vessels |
| diapedesis | wbcs squeeze through walls of blood cels to move to other surrounding body tissues |
| chemotaxis | movement of an organism or cell in response to a chemical |
| opsonization | opsonins tag a pathogen or dead cell for phagocytosis |
| natural killer cells | large granular lymphocytes, patrol body searcihing for pathogens and diseased host cells, attack and destroy |
| interferon | antimicrobial protein, secreted by virally infected cells and immune cells, alarm to nearby cells |
| complement system | group of 30+ globular proteins, contribute to innate immunity and adaptive immunity, synthesized in liver |
| classical pathway complement system | antibody binds to microbe, changes antibody's shape and exposes complement binding site, complement C1 binds and sets off complement fixation |
| alternative pathway complement system | complement C3b binds to microbe surface, activating reaction cascade |
| lectin pathway complement system | lectins bind to sugars on microbe surface, activates reaction cascade |
| lectin | plasma proteins that bind to carbs |
| inflammation | local defese against tissue injury, limits spread of pathogens and destroys them, redness, swelling, heat, pain, involves many cytokines |
| mobilization | local vasodilation from vasoactive chemicals, stimulate endothelial cells to contract, |
| firbinogen | forms sticky mesh around clots that walls off microbes |
| heparin | prevents clotting at site of injury (blod thinner) |
| tissue cleanup and repair | involves monocytes becoming macrophages, engulf and destroy bad cells, edema |
| pus | yellow accumulation of dead neutrophils, bacteria, cellular debris, tissue fluid |
| abscess | accumulation of pus in a tissue cavity |
| platelet derived growth factor | secreted by platelets and endothelial cells in injured area, stimulates fibroblasts to multiply, synthesizes collagen |
| hyperemia | excess of blood, delivers oxygen, amino acids, other necessities fo rprotein synthesis |
| pain | makes us limit use of a body part so it can heal uninterupted |
| pyrexia | fever, elevation of body temperature, systemic response, promotes interferon activity, elevates metabolic rate, inhibits producton of bacteria and viruses |
| pyrogen | resets the body's thermostat upwards |
| adaptive immunity | 3rd line of defense, systemic effect, exhibits specificity, has a memory |
| cellular immunity | T cells, lymphocytes directly attack and destroy foreign/diseased cells, gets rid of pathogens inaccessible to antibodies |
| humoral immunity | B cells, antibodies don't destroy but tag it for destruction, works for viruses, bacteria, yests, protozoans, etc. |
| natural active immunity | production of your own antibodies or T cells resulting from infection or exposure to antigens |
| artificial active immunity | productyion of your own antibodies or T cells resulting from a vaccination |
| natural passive immunity | temporary immunity from antibodies produced by someone else |
| artificial passive immunity | temporary immunity resulting from injection of antibodies from another person (immune serum) |
| epitopes | certain regions of an antigen molecule that stimulates an immune response |
| hapten | too small to be an entire antigen, may trigger an immune response by combining with a host molecule |
| MADGE | antibody classes, IgM, IgA, IgD, IgG, IgE |
| IgA | monomer in mucus and other secretions, pevents pathogen adherence to epithelia, passive immunity to newborns |
| IgD | monomer, B cell transmembrane antigen receptor |
| IgE | monomer, bound to receptors on basophils, mast cells, stimulates release of histamine and chemicals for allergies |
| IgG | monomer, 80% of circulating antibodies, can cross placenta to fetus |
| IgM | pentamer, large antibodies, first antibody released in immune response |
| T lymphocytes | T cells, adaptive immunity, 3 developmental stages |
| T cells stage 1 | birth in bone marrow |
| T cells stage 2 | training in thymus, positive selectuion, T cells become immunocompetent |
| immunocompetent | capable of recognizing antigens present |
| T cells stage 3 | deployment to carry out immune function, now naive lymphocytes that migrate to await their antigen |
| B lymphocytes | adaptive immunity, develop in red bone marrow, leave bone marrow to colonize lymphoid tissues and organs with T cells |
| cytotoxic T cells | carry out attack |
| heper T cells | promote activities for other immune cells |
| regulatory T cells | limit the immune response |
| memory T cells | responsible for memory in cellular immunity |
| MHC-1 proteins | occurs on all nucleated cells, internal peptides presented on cell surface, cytotoxic T cells respond |
| MHC-2 proteins | occur on APCs, external antigens presented on cell surface, heper T cells respond |
| T cell activation | heper or cytotoxic cells bind to MHC protein displaying and epitope, T cells undergoes mitosis, clone cells programed against same epitope, binds and delivers chemicals |
| B cell activation | antigen binds to B cell surface receptor, B cell digests the antigen, displays fragments and MHC-2 on surface, heper binds to MHC, B cell mitosis |
| B cell mitosis | some develop into memory cells, most become plasma cells |
| plasma cells PLAN | precipitation, lysis, agglutination, neutralization |
| neutralization | masking effective regions of an antigen |
| lysis/complement fixation | activation complement by classical pathway (cell lysis) |
| agglutination | clumping of enemy cells, immobilizing them |
| precipitation | antigen molecules are clumped by antibodies |
| primary response memory | immune reaction brought by first exposure to an antigen, delayed appearance of antibodies |
| secondary response memory | re-exposure to the same antigen, plasma cells form very quick, rapid antibody response, |
| hypersensitivity | excessive immune reaction against antibodies most people tolerate, includes alloimmunity, autoimmunity, allergies |
| type 1 hypersensitivity | acute, begins within seconds of exposure, secretion of histamine and inflammatory and vasoactive chemicals, trigger vasodilation, muscle spasms |
| type 2 hypersensitivity | subacute, antibody dependent, occurs when IgG or IgM attacks antigens bound to surface, ex. blood transfusion |
| type 3 hypersensitivity | subacute, forms antigen-antibody complexes, active complement triggers intense inflammation |
| type 4 hypersensitivity | delayed, cell mediated response, ex. TB test |
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