Immuno 2 Flashcards
(28 cards)
Type I Hypersensitivity
“Allergy” reaction
Is immediate type hypersensitivity
Antigen (allergen) triggers activation of TH2 CD4+ T helper cells leading to excessive production of IgE (via IL-4) by B cells
IgE binds and activates mast cells with release of mediators (e.g. histamine)
Large and widespread activation of mast cells can results in anaphylactic shock
Mast cells express the high affinity receptor for Fc portion of
IgE heavy chain – FcεRI
Once crossed linked, IgE promotes release of mast cell granules:
Histamine
Prostaglandins
Cytokines
Type II Hypersensitivity – subtype 1
Opsonization; phagocytosis
Cell is opsonized with autoantibodies and targeted for phagocytosis by neutrophils or macrophages
Typified by idiopathic/immune thrombocytopenia purpura
Type II Hypersensitivity – subtype 2
Complement-mediated / Inflammation
-Autoantibodies bound to cells or tissues activate complement-mediated inflammation
- Results in destruction of local area
Typified by Rh factor incompatability, Goodpasture syndrome
Type II Hypersensitivity – subtype 3
Antibody-mediated cellular dysfunction
Autoantibodies impair cell receptors or transmitter function without cellular phagocytosis or tissue inflammation
Typified by Graves disease or myasthenia gravis
Type III Hypersensitivity
Antigen-autoantibody immune complex disease
Large amounts of circulating immuno-complexes deposit in blood vessels and promote complement activation and inflammation
Depends on deposition of preformed immuno-complexes in vascular beds, organs (kidney), joints
Multimeric antigen-antibody complexes activate classical complement cascade
Typified by systemic lupus erythematosus & scleroderma
Type IV Hypersensitivity
T cell-mediated hypersensitivity in response to external/self Ag challenge in sensitized individual
- Delayed-type hypersensitivity, T-cell mediated inflammation/cytotoxicity
Reaction usually occurs 12-48 hours after exposure to antigen, peaks at 24-72 hrs
Perivascular accumulation of CD4+ helper TH1 cells & macrophages promotes cytokine secretion, increased vascular permeability, edema and fibrin deposition leading to tissue destruction
Typified by poison ivy reaction or positive response to common test for tuberculosis
Autoimmune Disorders typically seen in_______ and tend to present in _________.
women and Tend to present in adolescence or young adulthood.
Autoimmune disorders are linked to
HLA class II alleles, may be a hereditary component, may be triggered by earlier infections/injury
Which types of hypersensitivity are Autoimmune disorders?
Types II, III and IV hypersensitivity
Idiopathic thrombocytopenia purpura (Type II -1)
Platelets are anucleate cell fragments from megakaryoctyes that promote coagulation
- Thrombocytopenia is abnormally low number of platelets in blood
- Patients with
Goodpasture syndrome (II-2)
Autoantibodies to noncollagenous domain of the α3 chain of collagen IV (basement membrane) thereby destroying the epithelium
Graves disease (II-3)
In Graves, autoantibodies bind receptors on thyroid follicular cells mimicking TSH to maintain an activated thryoid state
Systemic lupus erythematosus (SLE) (Type III)
More common among women, onset in second & third decade
Deposition of immuno complexes in skin causes typical malar (butterfly) rash
Prevalence of antinuclear antibodies (ANA) – histones, dsDNA, RNP, etc
Systemic Sclerosis (SS) (III)
More common among women (50-60 years), fibrosing disorder
Clinically can lead to dysphagia (difficulty swallowing), joint destruction, pulmonary & kidney dysfunction
-can be diffuse or limited
Limited Systemic Sclerosis (SS)
Some patients have cryoglobulins producing Raynaud’s phenomenon
CREST syndrome scleroderma is associated with calcinosis (calcium deposits), Raynaud’s syndrome (cryoglobulins), esophageal dysmotility, sclerodactyly (hardening & tightening of skin), and telangiectasia (dilated superficial blood vessels).
Hyperacute rejection
Occurs within minutes to hours in presensitized pt
Interaction of preformed antibodies with proteins on surface of transplanted cells (ABO incompatible)
Clinically manifests with vascular disorders (acute arteritis, arteriolitis, thrombosis, ischemic necrosis)
Acute fibrinoid necrosis in blood vessel walls precipitating occlusion
Acute rejection
Occurs within days-months of transplantation in immunosuppressed pt
Can be either cellular or humoral immune based
Acute cellular rejection
Renal failure due to endothelitis
Clinically manifests as edema, interstitial hemorrhage & parenchymal tissue injury with mononuclear CD4+ & CD8+ T cellular infiltrate
Requires immunosuppressive therapy to maintain graft
Acute humoral rejection
Rejection necrotizing vasculitis promotes renal failure
Cell-mediated reaction initiated within days for organ transplant based on MHC mismatch
Requires immunosuppressive therapy to maintain graft
Chronic rejection
Intimal hyperplasia develops in graft blood vessels resulting in narrowing of graft vessels
Occurs over the course of years with loss of renal function
Not retarded by immunosuppression
Major cause of long-term graft failure is chronic rejection secondary to vascular stenosis and ischemia
Graft-versus-host
Occurs when donor lymphocytes respond to host MHC antigens
Commonly occurs in bone marrow transplantation
Inherited/congenital or acquired Immune defects can predispose to
infection, autoimmune disease and cancer
