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31 Cards in this Set
- Front
- Back
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Type I hypersensitivity (allergic)
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-first exposure: B cell secretes IgM -> 99% IgA 1%IgE
-IgE has special Fc part that attaches to mast cells -second exposure lead to allergic reaction -allergen must bind TWO IgE receptors simultaneously -triggers mast cells to release histamine granules, prostaglandins, and other cytokines |
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Why am i allergic to and you're not?
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-cytokines from an effector Th cell cause class
switching resulting in a clone of B cells destined to produce IgE -B cells differentiate into IgE-producing plasma cells and memory cells -IgE antibodies bind to mast cell receptors; the individual is sensitized (more mast cells) -cross-linking of cell-bound IgE causes the mast cell to degranulate -histamine and other mediators are released (you may not have B cells that recognize the antigen) |
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1st and 2nd differences:
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-you already have mast cell coded with IgE (2nd)
-antigen can bind to multiple receptors: T- independent response |
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Classic Type I HS
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-hives: "wheal and flare" around contact site
-hay fever: mucus membranes -asthma: leukotriene and prostaglandin, not treatable with antihistamine -generalized anaphylaxis: capillaries expand-> diapedesis-> hypovolemia-> shock-> death |
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Can you be "desensitized" to the allergen?
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-injected (not oral) allergen in small and gradually
increasing doses causes serum B cells to produce IgG -IgG competes with IgE for binding to allergen -anti-IgE antibodies: rhuMab for asthma |
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function of IgE
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-IgE bind to allergen and neutralize it
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Type II (cytotoxicity):
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-antibody mediated via complement or NK cells
ex) penicillin -small molecules (hapten) binds to cell surface, or cells with different (non-self) proteins are introduced into the blood (transfusion with wrong blood type) -antigen doesn't get recognized by immune system until hapten binds to the cell |
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Things happen when antibody binds to cells in your body
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-ADCC
-antibody activate complement system |
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Type III (immune complex disease):
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-mediated via Ag/Ab agglutination into complexes
-formation of immune complexes with slight antigen excess -immune complexes activate complement via classical pathway -immune complexes cannot phagocized -This causes basophils to degranulate, releasing mediators that increase vascular permeability (scale greatly exaggerated for clarity) -complexes circulate and are trapped in the basement membrane of small bv -activated complement attracts neutrophils and causes them to degranulate (C5a) -damage cells around capillaries |
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Type IV (cell-mediated, delayed)
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-mediated by Th cell + macropaghes
-response in days |
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sensitization with first exposure
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-Th cells become activated in normal way
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second exposure leads to reaction a few days later
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-effector Th cells secrete cytokines, activate macrophages, cause inflammation
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examples
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-poison ivy
-tissue transplant rejection -nerve damage in leprosy -metal "allergy" -TB skin test |
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anti-rejection drugs
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-cyclosporin: inhibits clonal expansion of T cells
-corticosteroids: reduce inflammation that causes tissue damage -basilixmab: blocks IL2 binding to T cells, so prevents activation of T cells by Th cell -Th cell doesn't activate other immune system |
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Autoimmune Diseases:
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-reactions to self antigens
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Myasthenia gravis
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-B cells recognize Ach receptors
-IgG neutralize Ach receptors- muscle can't contract -ptosis is one symptom |
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Type I diabetes
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-TCR on Tc cells recognize beta islet cells in pancreas
-beta islet produces insulin -beta islet are destroyed; no insulin is produced |
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Rheumatoid arthritis
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-Th cells recognize collagen in joints
:produce cytokines-> inflammation :activate B cells also recognize collagen and produce IgG against collagen(B cell clonal deletion not as rigorious) :immune complexes form-> Type III HS |
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Systemic Lupus Erythematosus
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-B cells recognize pieces of your own DNA (and other
self antigens) -IgG form immune complexes throughout the body, especially in capillaries -New Lupus Drug (benlysta) blocks stimulatory B-cell receptors to reduce B-cell clonal expansion |
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Hygiene hypothesis
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-autoimmune diseases are becoming more common
because we are "too clean"-having a robust population of native bacteria reduces autoimmune problems |
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treating autoimmune diseases by inducing oral tolerance
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-T reg cells reduce T cell responses by producing IL-10
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Potential therapeutic treatments:
Oral immunotherapy |
-eat the allergen to stimulate IgA and hopefully out-
compete the allergen |
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Anti-IgE (Xolair, omalizumab)
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-bind to the Fc part of free IgE to block binding to Mast Cells - more for asthma than food allergies
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Probiotic therapy
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-try to eat "good" bacteria (Bacteroides, Clostridia) to
allow increased production of T reg cells |
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Prebiotic therapy
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-feed your native flora; they like oligosaccharides even though humans don't digest them
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Immunodeficiency Diseases
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-failure to produce one more components of the
immune system |
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Primary: genetically inherited
SCID: |
-stem cells don't do VDJ joining- no B or T cells
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Agammaglobulinemia:
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-no B cells (X-linked disease)
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DiGeorge Syndrome:
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-no thymus= no T cells
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selective IgA deficiency
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most common
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Acquired
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-measles virus grows in T cells, weaken cellular immunity
-multiple myeloma is B cell cancer-one B cell proliferates at the expense of the others -HIV virus slowly destroys Th cells |
