Autoimmunity Flashcards
(38 cards)
your _____ immune system has 2 receptors ____ and _____, responsible for recognizing _______ of antigens
adaptive, immunoglobulin, TCR, 10^9 or more
there are ___ antigen receptor genes, ___ responsible for immunoglobulins _____, and ____ responsible for t cell receptor
7, 3, heavy, kappa lamda, 4 TCR: alpha, beta, gamma, delta
when apc presents to a naive tcell, it secretes ____ to turn it into a Th17 ____ to turn it into a Th1, and ____ to turn it into a Th2
TGFB, IL-6, IFN-gamma, IL-12, IL-4
Th17 cells turn on ____, Th1 cells turn on ____, Th2 cells turn on____
neutrophils, macrophages+mast cells, eosinophils
hypersensitivity is defined as:
injurious immune reactions (tissue injury as a direct result of your immune system)
definition of Type I hypersensitivity:
immediate, rapid immunologic reaction that occurs from previous sensitization, triggered by binding of antigen to IgE on mast cells
Type I Hypersensitivity pathogenesis:
initiated by introduction of allergen, stimulate Th2 responses and IgE production in genetically susceptible individuals (IgE class switching in B cells), re-exposure to allergen cross-links IgE and activates mast cells to secrete mediators
Cells associated with Type 1 Hypersensitivity
Mast cells (look like basophils deep blueish color) A in ACID mnemonic
in a slide of a type I hypersensitivity response, you see:
initially mast cells, later you see eosinophils
In a Type II hypersensitivity reaction:
antibodies react with antigens on cell surface or in the extracellular matrix causing disease by destroying cell, triggering inflammation, or interfering with normal functions (C in ACID, cy-TWO-toxic T cells)
pathogenesis of type II hs:
3 types: opsonization (direct coating of cell with antibodies and complement components, ingestion by phagocyte), inflammation (induced antibody deposition in fixed tissues i.e. basement membrane and extracellular matrix and by complement breakdown products i.e. glomerularnephritis, Cellular dysfunction from antireceptor antibodies that disturb the normal function of receptors i.e. myasthenia gravis, anti-TSH receptor activating TSH receptor in Graves causing hyperthyroidism
define Type III HS:
immune complex-mediated, antigen-antibody complex produces tissue damage by eliciting inflammation at the sites of deposition (I in ACID mnemonic “think 3 parts, antigen, antibody and complement protein”).
immune complexes are____ and _____ causing_____
insoluble, deposit in tissues, tissue damage via inflammation at the sites of deposition (usually at a site with lots of blood vessels), i.e. lupus- causing glomerular nephritis, complex gets lodged in the kidney
pathogenesis of Type 3 HS:
formation of immune complex (protein antigen triggers immune response, formation of antibodies) deposition of immune complex (deposited in blood vessels or tissues, organs where blood is filtered at high pressure, i.e. kidney), inflammation and tissue injury (activates complement system with release of breakdown products or engaging Tc receptors of leukocytes) this all results in vasculitis glomerulonephritis, and arthritis
Type 3, immune complex-mediated hypersensitivity, acute vasculitis, associated with necrosis of the vessel wall and intense neutrophilic infiltration
fibrinoid necrosis: necrotic tissue and deposits of immune complexes (the pink rink around vessel), inflamation. complement, and plasma protein area of tisue destruction, an apearance termed
Type 4 hypersensitivity is:
T-cell mediated
ACID: delayed (t-cell mediated)
inflammation resulting from cytokines produeced by CD4+T cells and cell killing CD8+T cells
RA, MS, Type 1 Diabetes, IBD,
type 1: immune system has turned on cytotoxic T cells to kill Beta islet cells in pancreas
Pathogenesis of Type 4 HS:
depends on type of cell turned on: 1 cytokine mediated: CD4+ t cells activated by exposure to antigen and differentiate into Th1 and Th17 effector cells
subsequent exposure results in cytokine secretion e.i. IFN-gamma activates macrophages to produce substances that cause tissue damage
2: cytotoxic reaciton: CD8+ cytotoxic T lymphocytes CTLs directly kill tissue cell (type 1 DM)
TB is a _____ hypersensitivity related to _____ cells
delayed-type, CD4 (Tuberculin PPD reaction)
ON TEST!
TB skin test is an example of:
Type 4, delayed-type hypersensitivity
positive PPD reaction,
during the Tuberculin PPD test, as the innoculation grows larger there are CD4 helper T cells that cause the inflammatory response
type I HS
ACID, A for allergy, anaphalaxis, bronchial Asthma
Immediate response,
production of IgE
autoimmune diseases def:, clinical features:
immune mediated damage of self tissues, clinical features: progressive with relapse and remission
Type 2 HS
ACID-C is for complement
antibody-mediated response
IgG, IgM, phagocytosis or lysis of target cell by activated comlement receptor,
autoimmune hemolytic anemia, myasthenia gravis, graves
Type 3 HS
ACID: I is for inflammation, Immune complex mediated
deposition of antigen-antibody comples into tissue, necrotizing vasculitis
SLE, Glomerulonephritis, serum sickness and arthus reaction
Type 4 HS:
ACID: D is for Delayed, activated T lymphocytes,
CD4 Tcell is making too much IFN-gamma recruites neutrophils or IL17 recruits macrophages
TB test, granuloma formulation, perivascular infiltrates,
MS, Type 1 diabetes, TB, Hashimoto’s thyroiditis
