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36 Cards in this Set
- Front
- Back
Type 1 HS (allergy)
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-IgE mediated
-sensitization with first exposure: IgA->IgE which attaches to mast cell -second exposure leads to allergic reaction:allergin binds to multiple IgE on the mast cell at the same time (like T-independent)->mast cells release their granules which include histamine and prostaglandins |
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IgE
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are created from IgM cells 1% of the time after first exposure and bind to mast cells, during the second exposure binds to allergin which causes the release of histamine and prostaglandins from mast cells like T-independent response
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Mast Cell
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are granules which release histamine and prostaglandins after antigens bind to the IgE receptors during second response which cause the allergic response
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Prostaglndin
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Are carried in mast cells and release during the second exposure when multiple IgE cells are bound to allergens
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Histamine
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Are carried in mast cells and release during the second exposure when multiple IgE cells are bound to allergens
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Leukotriene
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cause athsma when released with prostaglandins causing smooth muscle spasms=not treatable with antihistamines
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Sensitization
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induction of allergic responses
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Desensitization
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-injection of allergen into the blood stream in which we will mainly produce IgG because it is the serum antibody, enough IgG will bind to the allergin and neutralize it
-anti-IgE antibodies bind to the Fc part of IgE so it cannot bind to mast cells i.e rhuMab for athsma |
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Anaphylaxis
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-like septic shock
-peanut allergy -smooth muscle dilaters expand capillaries->diapedesis->hypovolemia->shock->death |
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Hay Fever
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-mucus membranes in nasal passages
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Type 2 HS (cytotoxic)
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-not an allergic rxn because it involves NK cells
-antibody is mediated by complement or NK cells -small molecule such as hapten is not recognized by our immune system until it binds to a cell and are introduced into the blood -classic example is hemolytic disease of the newborn |
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Hapten
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small molecule that is not recognized by our immune system until it binds to a cell
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ADCC
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NK bind to Fc part of an antigen whos Fab part is bound to a bacterium
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Hemolytic Disease of the Newborn
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-when mom is Rh- and dad is Rh+ so baby can be Rh+
-first born child's blood contacts the mother which elicits an immune response=ok -second Rh+ child will elicit a secondary immune response in mom and lots of IgG produced against the babies red blood cells -this is preventable by injecting anti-Rh antibodies during pregnancy and after each delivery: the IgG competes with Mom's B cells for the baby's blood and the mom is not sensitized i.e RhoGAM or Rhophyllac=essentially neutralizes the RBC |
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RhoGAM
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example of anti-Rh antibodies which neutralize the baby's red blood cells because it prevents the binding of Mom's B cells to the baby's RBC's
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Type 3 HS (immune complex)
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-mediated by antibody and antigen agglutination into complexes
-the antigen is in excess so we get immune complexes that are small and cannot be phagocytosed well so it activates the complement system and recruits neutrophils (C5a) which release granules that will cause cell death around them which kills the cells that line our capillaries -the tiny immune complexes get stuck in the basement membrane of our blood vessels which is worse than inflammation -i.e rheumatoid arthritis and lupus |
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Immune Complex
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-formed with agglutination of antibodies and antigen
-when antigen is in excess the immune complexes are small and are not phagocytosed well |
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Antigen Excess
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-causes formation of small immune complexes which are not phagocytosed well
-complement system gets activated which recruit the neutrophils C5a and they release granules which cause cell death around them which kill the cells that line our capillaries and the tiny immune complexes get stuck in the basement membrane of our blood vessels which is worse than inflammation |
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Basement Membrane
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-where the tiny immune complexes get stuck in our blood vessels which is worse than inflammation
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Neutrophil Degranulation
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-when the neutrophils (C5a) release granules which cause cell death around the cells that line our capillaries because of the excess of antigens
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Type 4 HS (delayed)
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-odd man out because its not mediated by antibodies
-mediated by Th cells and macrophages -response peaks in days, not minutes -sensitization with first exposure and Th cells become activated normally -second exposure which happens a few days later: effector Th cells secrete cytokines and activate macrophages which cause inflammation -i.e poison ivy, tissue rejection, nerve damage in leprosy, metal allergy, TB skin test |
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Cell-mediated HS
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type 4 hypersensitivity
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Inflammation
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because of activation of macrophages from effector Th cells that secrete cytokines
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Anti-rejection Drugs
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cause patient to be immunocompromised
-cyclosporin:inhibits clonal expansion of T cells -corticosteroids: reduce inflammation that causes tissue damage -basiliximab: blocks IL-2 binding to T cells so prevents activation of T cells by Th cells |
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Autoimmune disease
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-reactions to self antigens
-myasthenia gravis and Type 1 diabetes |
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Myasthenia Gravis
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-B cells recognize ach receptors
-IgG neutralizes the AcH receptors and the AcH cannot bind to the muscle cell receptor and the muscles cannot contract -ptosis is one symptom |
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Type 1 diabetes
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-T cell receptors on T c cells recognize beta islet cells in the pancreas and the beta cells are destroyed which causes no production of insulin
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Rheumatoid Arthritis
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-Type 3 HS
-Th cells recognize collagen in joints which produce cytokines and cause inflammation (type 4 HS), activate B cells that may recognize collagen also and produce IgG against our collagen and immune complexes form |
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Lupus
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-B cells recognize pieces of our own DNA
-IgG form immune complexes throughout the body, especially in capillaries -butterfly rash -benlysta blocks stimulatory B cell receptors to reduce B cell clonal expansion |
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Hygiene Hypothesis
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-Relation of Treg cells, pathogen>native flora, and autoimmune problems
-too clean explains why we dont have native flora, too few T reg cells, increase in autoimmune disease -bacteria in our gut is important and happens early -leads to idea of treating autoimmune diseases by inducing oral tolerance which stimulates production of T reg cells and secrete IL-10 |
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Oral Tolerance
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treating autoimmune diseases by inducing oral tolerance which stimulates production of T reg cells and secrete IL-10
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Probiotic
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-try to eat good bacteria that contains bacteroides and clostridia to allow increased production of T reg cells
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Prebiotic
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-not proven useful in adults
-feed our native flora with oligosaccharides from breast milk |
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Immunodeficiency Diseases
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failure to produce one or more components of the immune system
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Inherited IDD
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-SCID: stem cells dont do VDJ joining-no B or T cells
-Agammaglobulinemia: no B cells (x-linked disease) -DiGeorge Syndrome: no thymus=no T cells -Selective IgA deficiency: most common gentically inherited IDD |
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Acquired IDD
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-measles: virus grows in T cells and weakens our cellular immunity
-multiple myeloma: B cell cancer, one B cell proliferates at the expense of the others -HIV virus: slowly destroys Th cells |