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patho ch 4
| Term | Definition |
|---|---|
| Immunity | Body's ability to recognize and neutralize harmful agents |
| Innate immunity | nonspecific response |
| Adaptive immunity | specific responses |
| Antigen Presenting Cell | cell that displays antigen to activate T-cells example include macrophage/dendritic cells |
| T-lymphocytes (what is main function) | mediates cell mediated immunity |
| B-Lymphocytes | produce specific antibodies, important in humeral immunity |
| Humoral immunity | antibody mediated immunity, B-cells |
| Alloimmunity | immune response to antigens from another person ie. graft rejection (host vs. graft), GVHD (graft vs host), blood transfusion reaction |
| CD4 | Helper T Cells, regulates immune responses and activate B-cell/macrophage/other immune cells |
| Helper T Cells (called) | CD4 |
| CD8 | cytotoxic T Cells, kills infected or abnormal cells directly |
| Cytokine | signaling proteins that can activate inflammatory process and immune response |
| Major Cells of innate immunity | neutrophil, macrophages -- it does not have memory |
| Major cells of Adaptive Immunity | T Cells, B Cells, these cells have memory (in form of Ag/Ab recognition) |
| Neutrophils | first responder of immune system, phagocytize pathogens/debris |
| Macrophages | mature monocytes that engulf pathogens and present Ag to lymphocytes |
| Dendritic Cells | Capture Ag and present to T-cells to start ADAPTIVE immune response |
| natural killer (NK) cells | recognize/kill virus infected or abnormal cells without prior sensitization |
| CD8 cells are also called | cytotoxic T-cells |
| B-lymphocytes are developed in | B is for bones |
| T-lymphocytes are developed in | T for thymus coordinate cellular immune response |
| Central (primary) lymphoid organ | thymus/bone marrow |
| Peripheral (secondary) lymphoid organ | lymph nodes, spleen, tonsil initiation sites of immune response |
| Lymph fluid | transportation of immune cells and Ag between tissue/lymph organs |
| MHC Class I | Present to CD8+ cells |
| MHC Class II | Present to CD4+ cells |
| How do lymphocytes have memory | B and T cells express unique receptors for a single specific antigen |
| Clonal selection | Ag binds to matching lymphocytes and activate immune response |
| Clonal expansion | activated cells quickly proliferate to respond to Ag |
| Memory cells | subset of B-lymphocytes with long life and can start stronger/faster response in the future |
| IgG | most abundant immunoglobin crosses placenta to provide passive immunity to babies |
| IgA | found in mucosa and breast milk |
| IgM | first Ab made in response to pathogen exposure ie HAV IgM |
| IgE | trigger allergic reaction |
| IgD | initiate B-cell activation |
| Antibody action by steps | 1. neutralization 2. opsonization 3. complement activation |
| neutralization step | Ab binding to virus/toxin to block interaction with host cell step 1 of Ab action |
| opsonization step | Ab coat pathogens and tag for destruction by phagocytes step 2 of Ab action |
| complement activation step | Ab activate complement cascade and enhance inflammation and immune response leading to cell lysis step 3 of Ab reaction |
| TH1 cells | CD4+ subset cell stimulate macrophage to attack pathogen |
| TH2 cells | stimulate B-cells to enhance Ab production especially with parasite and allergens |
| TH1/TH2 balance | impact autoimmune disease risk/allergies |
| TH1 dominant responses means | critical for clearing intracellular infection can contribute to autoimmune disease |
| TH2 dominant responses means | promote strong Ab production increase risk for allergies or asthma |
| T cell receptor | receptors on T-cells that recognize Ag from MHC complexes |
| what does too small of an immune response mean | immunodeficiency and reduced ability to detect abnormal cells (ie. cancer) |
| what does too big of an immune response mean | allergy (hypersensitivity reactions) or autoimmune disease |
| primary immunodeficiency | inherited or congenital example is severe combined immunodeficiency (SCID) |
| SCID | severe combined immunodeficiency, primary immunodeficiency T/B-cell function are impaired |
| Secondary immunodeficiency | acquired later in life ie. HIV or chemotherapy |
| Antigenic variation | rapid mutation leading to surface protein changes --> antibodies are unable to recognize ie. influenza |
| latency | pathogens can go dormant and reactivate later ie. herpes simplex or HIV |
| immune system hijack | directly infect/disable immune cells ie. HIV infects CD4 and cripples immune responses |
| Type I hypersensitivity reaction | IgE mediated binding to mast cells and basophils triggering histamine/leukotriene (rapid onset) ie. anaphylaxis or allergy |
| Type II hypersensitivity reaction | Ab (IgG or IgM) reacts against self antigens causing cell lysis via complement or phagocytosis ie. hemolytic anemia, transfusion reaction, graves disease |
| Type III hypersensitivity reaction | immune complex deposition (Ab-Ag complexes) in tissues which activates complement causing inflammation ie. systemic lupus erythamatosus, serum sickness |
| Type IV hypersensitivity reaction | T-cell mediated hypersensitivity reaction (delayed hypersensitivity), may have inflammatory response ie. TB test or contact dermatitis (like poison ivy) |
| autoimmunity | failure to recognize self may involve molecular mimicry or loss of tolerance and is usually organ specific genetic predisposition or environmental impact ie. graves or SLE |
| what are some methods to suppress immune response | corticosteroids, cytotoxic drugs, biologics |
| cytotoxic drugs | inhibit proliferation of immune cells ie. chemotherapy, methotrexate, azothiaprine |
| biologics | block cytokines ie. anti-TNF drugs |
| AIDS | target CD4 decreased cell mediated immunity and humoral immunity (2 methods of attack remember) increased risk of opportunistic infection |
| how is AIDs diagnosed | viral load and CD4+ count (<200) |
| how is aids treated | with antiretroviral medications ie. truvada (Emtricitabine/tenofovir) |
| anaphylaxis | type 1 sensitivity reaction (rapid IgE mediated resposne) vasodilation (decreased BP), bronchospasm and hypotension, swelling in mouth |
| how is anaphylaxis treated | epinephrine, fluids, antihistamines |
| SLE | systemic lupus erythematosus (type 3 reaction) autoantibodies cause systemic inflammation (small blood vessels, organs, skin, joint, CNS, kidneys) |
| how is SLE diagnosed | ANA, anti-dsDNA and low C3/C4 complements |
| how is SLE treated | steroids and immunosuppressants |
| what do vaccines stimulate | adaptive immunity (dont cause illness and leads to fast response to pathogen) |
| type of vaccines | mRNA, attenuated, inactivated, conjugate |
Created by:
sleepingbear
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