Vaccines
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| Passive immunization | immediate. no induction of immune response. temporary. combinations used. risk of type 3 hypersensitivity anytime you immunize. you always actively immunize when you passively immunize.
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| Active Immunization | Induce Immune Response (CTL). long lasting protection. stimulate neutralizing Abs. provide protection without causing disease. economically feasible.
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| Herd Immunity | As fraction of pop that is vaccinated increases, chances of an infectious agent finding an unprotected individual becomes smaller. leaving population resistant as a whole.
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| Live Attenuated Vaccines. | Replicate in recipient(KEY fact). has been genetically altered so it doesn't cause disease. proteins produced are turned over as well. adaptive immune response that is complete. Cd4,Cd8,Memory,Nk. ONLY ONE YOU GET CTL for. can be painful.
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| Killed Vaccines | whole organisms. No multiplication. complete microbe. CD4 T cells. No cell mediated immunity. Require multiple doses. advantage = whole organism has bacterial + viral components act as adjuvant.
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| Extract Vaccines | Not whole organism. individual components. need booster doses. disrupted or lysed cells. only adjuvant you use is aluminum derivatives. meant to keep Ag in body longer.
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| Vaccine Conjugates | For encapsulated bacteria. Have polysaccharide capsule. not held well by MHCII molecules. conjugate to large globular protein, usually toxoid. you activate b cell specific for disease, take in, present all different epitopes on surface.
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| Once you have the T cell specific for the toxoid epitope, what happens? | The 2nd signal is given. B cell produces Abs for the toxoid and for the pathogen. T cell will release cytokines for class switching, can produce IgG and IgM.
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| Toxoid | Chemically modified toxins, harmless.
used when pathogenicity of an organism is due to the toxin.
diphtheria and tetanus
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| Central tolerance | negative selection. 1* lymphoid organs. eliminate b and t cells that ind to self, become anergic, die.
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| peripheral tolerance | 2* lymphoid organ. Results in anergy or suppression.
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| Anergy in peripheral tolerance | TCR has receptor for self antigen. comes in contact with self antigen. Not an APC, so no B7 or IL-1. anergic. Only one signal.
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| Suppression in peripheral tolerance | T suppressor cells and T regulatory cells
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| T suppressor Cell | Subset of CD4 cells. express CD25 that downregulates T cell, active following immune response.
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| T regulatory Cell | Turn off and downregulate any potential autoreactive cell that may have become activated.
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| What causes breakdown of tolerance? | spontaneous. infection associated. environmental and genetic factors. linkage with certain MHC alleles, hormonal factors; estrogen and progesterone influence.
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| Mechanisms involved in loss of self tolerance | 1) Escape of autoreactive b/T cells
2) bystander effect
3) Molecular mimicry
4) epitope spreading
5) release of normally sequestered antigens
6) loss of suppression
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| Bystander Effect | Come in contact with Self-Ag, no 2nd signal. In an area where immune response is occuring, can become activated due to cytokines being released in the area for other infections. superantigen is an example of this.
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| Molecular mimicry | Mount Immune response to microbes. Tcells and Ab structurally similar to self protein, cross react, cause damage.
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| Diabetes | molecular mimicry. Coxackie virus. CMV cross reacts with glutamate decarboxlyase present on beta islet cells of pancreas.
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| Epitope spreading | Damage exposes self epitopes that weren't there originally. they look new to the body, like foreign Ag.
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| Myesthenia Gravis | Type II Hypersensitivity. Abs to Ach receptor. blocks function. Abs now elicit destruction of receptor and internalization, leaving less on the surface. AchAse inhibitors and azothioprine (immunosuppressant drugs).
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| Graves disease | Type II Hypersens. Abs to TSH receptor. increase of thyroxine. Hyperthyroidism.
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| Warm Autoimmune hemolytic Anemia | Type II Hypersens. IgG to RhD antigen. molecular mimicry. Cross react with RhD. destroyed by opsonization. in body at warm temps.
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| Cold autoimmune hemolytic anemia | IgM to glycophorin. all over surface of RBC. binds IgM. destroyed by complement. Only binds at cooler temps. seen in hand and feet. If you warm up, Abs detach from RBCs.
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| Rheumatic Fever | Type II Hypersens. Abs against group A strep cross react with heart myosin.
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| Goodpastures Syndrome | Type II Hypersens. Abs to type Iv Collagen. binding to Bm of glomeruli.
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| Rheumatoid Arthritis | Type III Hypersens. Ab/Ag complexes. abnormal IgG against virus/bacteria. IgM attacks the FC region of that. precipitates. C3a and c5a can keep reacion sustained.
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| Systemic Lupus Erythematosus (SLE) | Type III Hypersensitivity
antibodies against ANA DS DNA. activate complement. butterfly rash.
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| SLE Mechanism | IgG and IgM against nuclear antigens. DsDNA, histones, RNP, phospholipids.
they deposit in BV, kidneys, CT, skin, induce complement, inflammation.
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| Factors of SLE Induction | CD4 t cells for nucleosomal antigens escape. UV radiation inducs apoptosis, alter dna structure so it looks foreign. HLA-DQ alleles associated.
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| Multiple Sclerosis | Type IV. demyelinating. Progressive. alterations in T cell and cytokines. to myelin basic protein, adenovirus, hhv6, epstein barr. T cells and Abs cross react with myelin.
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| hashimoto's t hyroiditis | destroy thyroid. lymphocyte infiltration. CD4+ T cells and autoabs to thyroglobulin. hypothyroidism. Goiter
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| Celiac Disease | MHCII DQ2 and DQ8 Alleles.
Develop Anti-gliadin IgA, Anti-tTG Iga, Anti-endomesium IgA.
Th1- mediate inflammatory response
TH2 - activate B cells, autoantibodies.
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| how to diagnose Celiacs Disease? | Anti-tTG IGA
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| Why is celiac disease associated with dermatitis herpetiformis | Develop IgA to wheat protein gliadin
Ab cross react with reticulin - subepidermal blistering.
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