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L6 Hypersensitivity

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undesirable, damaging, discomfort-producing and sometimes fatal reactions produced by the normal immune system (directed against *innocuous antigens*) in a *pre-sensitised* (immune) host
IgE mediated mast cell and basophil degranulation & cross linking of FcR by allergen -> release of preformed (e.g. histamine) and de novo synthesised (e.g. leukotrienes) inflammatory mediators; CLINICAL FEATURES: fast onset, weal and flare, can have 2nd phase (late) response; COMMON ANTIGENS: pollen, bee venom, animal dander; ASSOCIATED DISEASES: hayfever, allergic asthma, rhinitis, dermatitis food allergy; severe reaction = ANAPHYLAXIS
Immunoglobulin E
produced by plasma cells from class-switched B cells under control of IL-4 and CD40L-CD40 interaction; extremely low serum levels but high affinity for FcR on mast cells and basophils - permits stable binding over long periods
pre-formed mediator: stimulates irritant nerve receptors, smooth muscle contraction & increases vascular permeability
pre-formed mediator: activates bradykinin - similar action to histamine
pre-formed mediator: role unclear
arachidonic acid
lipid (secondary/late phase) mediators: leukotrienes & prostaglandins are derivatives of...
late-phase response: similar properties to mast cells over longer time scale
late-phase response: granules contain cytotoxic proteins (e.g. ECP); attracted to sites of allergic inflammation by CHEMOKINES (Eoxtaxin1/2); in tissues, release contents of granules -> major source of tissue damage in allergic response
T cell responses
late-phase response: involved in both late and early response to allergen; cytokine production by activated cells critical in ongoing response; cytokine-driven activity is major source of pathogenesis in allergic response
antibody-mediated cytotoxic reactions; binding of antibody to target antigen on cell membrane results in: activation of complement cascade resulting in cell lysis; aggregation of Fc portions of immunoglobulin/C3b with binding to FcRs/C3bR resulting in opsonisation, phagocytosis & destruction; initiated by IgM or complement-binding IgG (IgM >> IgG); EXAMPLES: blood group incompatibility, autoimmune haemolytic anaemias, affecting neutrophils, affecting platelets
most efficient at mediating Type II cytotoxic reactions as they are pentavalent
require multiple binding to mediate Type II cytotoxic reactions
haematopoietic cells
cells most commonly affected by type II (cytotoxic) hypersensitivity reactions
ANTIBODY MEDIATED IMMUNOPATHOLOGY: Immune Complex Reactions: 1) IgG + Ag = AgAb complex; 2) FcR in complex bind C1q; 3) complement activation produces activated complement fragments; 4) C5b attracts neutrophils & C3b opsonises; 5) attempted phagocytosis of complexes - release of enzymes and oxygen radicals; 6) consequence is TISSUE DAMAGE
results from Type III hypersensitivity in blood vessel endothelium
results from Type III hypersensitivity in renal glomeruli
results from Type III hypersensitivity in joint spaces
Arthus reaction
results from Type III hypersensitivity in perivascular area
Farmer's lung
results from Type III hypersensitivity in alveolar/capillary interface
Intrinsic factor
can be directly inactivated by antibodies, leading to B12 deficiency (Type III hypersensitivity)
Myasthenia Gravis
inactivation of AChR due to receptor blockade by antibodies occurs in _______ _______ (Type II hypersensitivity)
CELL MEDIATED IMMUNPATHOLOGY: T cell mediated - CD4+ (MHC Class II); delayed type e.g. Tuberculin skin reaction; initially perivascular infiltration of lymphocytes/monocytes; LANGERHAN'S cells present neo-antigen to T cells; Ag-specifc T cells release cytokines - recruitment of non-specific macrophages, which cause tissue damage; requires previous exposure to antigen
Contact dermatitis
Type IV hypersensitivity: T cell mediated cytotoxicity (CD8+ (MHC Class I)); e.g. NICKEL, POISON IVY; combination of DTH and cytotoxic reaction; Nickel acts as hapten with epidermal proteins; antigen presentation by APC; Keratinocytes may present to CTL precursors
Focal collections of inflammatory cells in tissues: macrophages, epithelioid cells (phagocytic cells containing foreign material), giant cells, lymphocytes; T cells are Th1 type (secrete IL2 & IFNy); release of IL-12 by macrophages critical in initiation of response
granulomatous diseases
Examples of __________ ________: mycobacterial infections (TB, atypical mycobacteria, leprosy) & unknown aetiology (Sarcoidosis, Wgener's granulamatosis, Crohn's disease)
Tuberculoid leprosy
in patients where Th1 response occurs - protective (successful mounting of effective immune response)
Lepromatous leprosy
in patients where Th2 response occurs - non-protective (failure to mount effective immune response)