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Acquire Immunity
Micro 1113
| Question | Answer |
|---|---|
| What are the 3 characteristics of aquired immunity? | 1.Displays specificity-only immune to 1 specific disease2.Displays memory-"remembers" how to defend3.Recognizes "self" from "non self" |
| Humoral Immunity | 1.antiboy mediated immunity, AB is involoved, AB molecule is protective |
| Cell mediated Innumity | CMI- immunity is affected by cells, not AB 2.Cells produce the protection |
| Antibody | (HI) proteins produced by an individual in response to an antigen. Proteins molecular weight are of 160,000-900,000Thare are found in the body fluids (serum,plasma,lymph,mucous, csf, synovial fluids etc)Can be isolated from serum by electrophoresis |
| Antigens | molecules that induce AB formation. They are1.proteins, polysaccharides, and sometimes lipids or nucleic acids.2.must be larger than 10,000 D molecular weight3.Usually foreign to an individual and may be part of an IA. |
| Antigenic determinant | eiptopes, little bumps on an AG's surface that determine the AB it will combine to. |
| Describe the structure of and AB | Proteins composed of two identical polypeptides called heavy cahins and two identical, but hsorter, polypeptides called light chians and are covalently linked together. |
| Immunoglobulin G | (IgG) 1 class of AB molecules that are in highest concentraion in blood2 heavy chains, 2 light chains, 2 ab comb sites are identicleprotects from disease |
| IgM | Largest ab molecule, next highest in concentraion2.10 ag combining sites |
| IgA | ab found in mucous secretions2.protects from secretory diseases4 ab combing sites |
| IgD | Unkown function2 ab combining sites |
| IgE | lowest concentration, responsible for allergiesprotects from worms2 ab combining sites |
| What is the origin of immunoglobulins? | They are produced by cells derived from stem cells of the bone marrow |
| B-Cells | mature into bone marrow and are responsible for HI |
| T-Cells | migrate to and mature in the thymus, they are responsible for CMI |
| Amamnestic immune response | 1.on re-exposure of the same ag, the immune response occurs more quickly and produces more Ab2.This is due to MANY memory cells3.This is the basis for memory; the second immune response is quicker and more intense |
| Precipitation tests (Immunoelectrophoresis) | 1.the ag is soluble, it's soultion is clear2.Ab-Ag comples produces a visible precipitate |
| Aggulation test | The Ag is BIG, it's suspension is cloudy2.particulate ag forms visible clumps |
| Enzyzmy-linked immunosorbant assay | ELISA1.Ag is absorbed to surface2.A human Ab is added (serum)3.Human Ab is detected by the used of an enzyme linked to an Ab specific to the human Ab |
| Fluorescent Ab | 1.A fluorescent chemical is linked to an Ab2.The Ag is detected by fluorescence mictoscopy |
| Ab Titer | 1.A measure of the amount of Ab in an individuals serum2.May indicate stage of disease or the severity of diseasein an individual. |
| How do Ab protect against disease? | Neutralize exotoxins, attach to extracellular parasites (this is called opsonization), attach to viruses and prevent their attachment and entrance into host cells (virus neutralization) activate complament. |
| Oposonization | Ab's can attatch to a cell capsule which prevents phagocytosis and allows wbc's to attack bacteria |
| Active, natural immunity | a.aquired by surviving an infectionb.a natural processc.the individual produces the immunityc.immunity is long lived, memory cells are present |
| Passive, natural immunity | a.immunity of a newborn infantb.a natural processc.the child recieves immunity made by it's motherc. mediated by IgG that has crossed the placentae.short lived, no memory cells |
| Active, artificial immunity | (vaccinations)a.acquired by immunizationsb.artificialc.immunization causes host to make Ab'sd.Immunity is long lived, memory cells are present |
| Vaccines may be....... | 1.killed cells or inactivated virus2.component(s) of bacterial cell wall3.Toxoids (denatured exotoxins)4.Attenuated bacterial cell or virus, these are alive but altered in some way as to enable them from causing pathology. |
| Passive, artificial immunity | (plasma induced)1.acquired after administration of gamma globulin2.artificial3.Ab's are made by donors, individual receives Ab's does not make Ab's.4.Sort lived, memory cells are NOT present, immunity is short lived (3-6 mos) |
| Dep B Vaccine and schedule | Viral surface proteinBirth, 1-5 mos, 5-20 mos |
| Diptheria, Tetanus, and Pertussis (DTP) | D-toxoidt=toxoidp=component2,4,6 mos 14-20 mos and 4-6 years |
| Meningitis and H. Influenzae | Conjugated capsule2,4,6 mos 12-16 mos |
| Polio | Inactivated virus (IPV)2,4,6-20 mos and 4-6 years |
| meningitis and S.pneumoniae | capsule2,4,6,12-15 mos |
| Measles, Mumps, and Rubella | (MMR)attenuated viruses (little pieces)12-16 mos and 4-6 years |
| Chicken Pox | attenuated virus12-20 mos |
| hep A | Inactive virus>24 years of age |
| Cell Mediated Immunity | T-Cells;are protective against intracellular parasites such as viruses and bacteria that have entered cell hosts and Ab's cannot reach them. |
| Helper T-Cells | Secrete lymphokines that induce inflammation and activeate macrophages enhancing metabolism so intracellular microorganisms can be killed. |
| Cytotoxic T cells | they react with and Ag on infected cells causing their destruction |
| Memory Cells | A helper t cell that reacts like original T-Cells |
| Type I hypersensitivity disease (immediate) | 1.Allergies2. Pahtologya.IgE is produced in response to an Agb.IgE binds to mast and basos c.on reaction with allergen, cells secrete mediators such as histamine causing contraction of SM, dilation of capillaries, and inflamation |
| What are ways to treat allergies? (IgE) | avoidance of allergens, drugs that neutralize mediators or prevent their action such as antihistamins, and immunization with allergen to produce IgG Ab's which neutralize allergen before it reacts with IgE |
| Tyoe II sensitivity disease (cytotoxic) | 1.IgG or IgM Ab's involved2.Ag is part of call3.Reaction of Ab with Ag on cell causes destruction |
| Examples or Type II hypersensitivity reactions | 1.Blood transfusion incompatibility reactions2.Hemolytic disease of newborn (Rh factore) |
| Type III hypersensitivty disease (complex-mediated) | 1.IgG and IgM2.Ag is not part of cell (soluble)3.pathology- Ab-Ag complex formed and filiter into kidney and organs, activate complement, induces inflamation and results in pathology.ex-glomerulonephritis-inflamation in the kidneys and arthritis-inf |
| Type IV hypersensitivity (cell mediate, delayed) | 1.T-Cell involvment2.Contact sensitivity (poison ivy, oak, nickel, latex etc)2.On contact Ag reacts with T Cell causing proliferation3.on re-exposure to Ag, many tcells release lymphokines causing symptoms. |
| Autoimmune Disease | Pathology caused by an immune response top a person's own Ag's (tissue) |
| Myasthenia Gravis (cytotoxic II) | 1.Ab reacts with receptors at myoneural junction which eliminates receptors2.Muscle contraction is weak |
| Insulin Dependent Diabetes Melitis (Type I, juvenile onset) | 1.An immune response occurs against Ag's on beta cells, the source of insulin2.Causes destruction of the beta cells; this results in diabetes |
| Systemic Lupus Erythematosus (SLE, Lupus) | Complex mediated, Ab to DNA or cell nucleus activation of comp.1.Ab reacts to individuals own nucleic acid and/or cell structure2.Ab and Ag form immune complexes and wherever these form, complement is activated causing inflamation and damage |
| Rheumatoid Arthirisis | 1.Ab reacts with an individual's own Ab's2.Complexes formed, usually in joints, activates complement, which results in inflammation in joints.3.The chronic joing inflammation causes continued damage and disfigurement of joints |
| Multiple Sclerosis (MS) | 1.Caused by an immune respone, probably mediated by T-Cells, that attacks myelin cehaths that surround nerves2. Destruction of myelin results in slow nerve impulse conduction and loos of muscle function.3.Occurs in colder climates although it is not a |
| Causes of autoimmune diseases? | 1.mostly unkown2.May be a result of viral or bacterial infection3.Genetic inheritance omay predispose to autoimmune disease4.Combination of any of these causes |
| Treatment of autoimmune diseases | 1.suppression of immune response by administration of coritsone/prednisone or cytotoxic drugs2.Removal of Ab's by plasmapheresis3.Administration of antiinflammatory agents |
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MyKidzRKute
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