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44 Cards in this Set

  • Front
  • Back
What is another name for type I hypersensitivity disorders?
anaphylactic type
What is the basic sequence of events in type I hypersensitivity reactions?
-antigen stimulates TH2 cells to produce cytokines (IL-4, IL-5), which stimulates B cells to make IgE
-IgE binds to high affinity Fc receptors of basophils and mast cells
-upon 2nd exposure, antigen reacts w/and crosslinks bound IgE
-results in degranulation and release of histamine, production of cytokines, and activation of phospholipase A2
What effect do histamine and other vasoactive substances have on the body?
cause vasodilation, vascular leakage, and smooth muscle spasm (occurs 5-30mins after exposure)
What is the "late-phase" of type I hypersensitivity reactions?
2-8days later, recruitment/infiltration of eosinophils, neutrophils, basophils, monocytes; tissue damage

*see tissue and peripheral blood eosinophilia*
What are some examples of local type I hypersensitivity reactions?
allergic/atopic rxns: seasonal rhinitis (hay fever), allergic asthma, urticaria (hives)
What are the symptoms associated with systemic anaphylaxis?
(aka anaphylactic shock)
rapid urticaria, bronchospasm, laryngeal edema, and shock
What are the "secondary mediators" of an anaphylactic reaction?
leukotrienes B4, C4, D4, prostaglandin D2, PAF (all produced from activation of arachidonic acid pathway), and cytokines (to contribute to immune response)
What is another name for type II hypersensitivity disorders?
cytotoxic, or antibody dependent
What is the key characteristic of the antigens in type II hypersensitivity reactions?
they are INTRINSIC TO THE CELL OR TISSUE that is damaged (usu either altered or normal cell membrane components)
What are the 3 different types of antibody dependent hypersensitivity reactions?
1. complement-fixing antibodies
2. antibody-dependent cell-mediated cytotoxicity (ADCC)
3. reaction of anti-receptor antibodies with cell-surface receptors
What happens in complement-mediated cytotoxicity?
antibody reacts with cell surface antigen, leading to fixation of complement and cell lysis (also opsonizes cells for phagocytosis)
What are the common examples of complement-mediated cytotoxicity?
-autoimmune hemolytic anemia (develop antibodies against your OWN blood)
-hemolytic transfusion reactions (incompatible ABO)
-erythroblastosis fetalis(rhesus incompatibility)
-Goodpasture syndrome (antibodies against glomerular and pulmonary alveolar basement membranes)
What happens in antibody-dependent cell-mediated cytotoxicity (ADCC)?
antibody binds to integral cell surface antigen, and cytotoxic leukocytes then react with the Fc portion, which lyse target (usu NK cells, but also monocytes, neutrophils, and eosinophils)
What happens in antibody-mediated cellular dysfunction?
antibodies form against integral surface receptors that impair or dysregulate fn (w/o causing inflammation or injury)
What are the most common forms of antibody-mediated cellular dysfunction?
Graves disease -> antibodies stimulate TSH receptor, causing glandular hyperplasia and hyperthyroidism
Myasthenia gravis -> antibodies against ACh receptor in motor end plates cause muscle weakness
What is another name for type III hypersensitivity reactions?
immune complex mediated reactions
What is the key characteristic of the antigen in type III reactions that differs from the antigen in type II reactions?
type III: antigen is NOT an intrinsic component of target cells (but can be endogenous or exogenous)
type II: antigen must be intrinsic component of target cells
What is the basic mechanism of type III hypersensitivity reactions?
1. antigen stimulates antibody production, and antigen-antibody complexes are formed in circulation
2. antigen-Ab complexes get deposited in tissues (vessel walls, serosal surfaces, extravascular sites)
3. initiates inflammatory reaction
What are the 3 main components/pathways that contribute to the inflammatory response in type III hypersensitivity reactions?
1. complement activation
2. platelet aggregation
3. activation of Hageman factor (XII)
What are the downstream effects of complement activation in type III reactions?
release anaphylatoxins (C3a/C5a) -> release vasoactive amines -> vasodilation and edema

release chemotactic factors (C5a) -> attracts neutrophils -> phagocytose the complexes -> release lysosomal enzymes -> necrosis
What are the downstream effects of platelet aggregation in type III reactions?
microthrombi formation -> ischemia -> necrosis
What are the downstream effects of the activation of Hageman factor in type III reactions?
microthrombi formation -> ischemia -> necrosis

activation of kinins -> vasodilation and edema
Why don't these antigen-antibody complexes get removed by mononuclear phagocytotic cells, like normal?
smaller immune complexes are less readily removed, sometimes there is overload or dysfn of mononuc phagocytotic system
What are some examples of type III hypersensitivity reactions?
-serum sickness (react a/g horse serum; systemic deposition complexes esp in heart, joints, kidney)
-systemic lupus erythematosus (also multisystemic)
-arthus reaction (local)
-polyarteritis nodosa (generalized, involving small/medium arteries)
-immune complex-mediated glomerular diseases
What is the Arthus reaction?
localized area of tissue necrosis from acute immune complex vasculitis; exogenous antigen is introduced (injection or transplant) and reacts w/PREFORMED antibodies
What are some different types of immune-complex mediated glomerular diseases?
poststreptococcal glomerulonephritis, membranous glomerulonephritis, lupus nephropathy
What is another name for type IV hypersensitivity reactions?
What are the 2 main types of cell mediated hypersensitivity reactions?
delayed-type (mediated by CD4 cells) and CTL-mediated cytotoxicity (mediated by CD8 cells)
What is the mechanism in delayed-type hypersensitivity?
1st exposure: antigen recognition, results in memory TH1 CD4 cells
re-exposure: memory TH1 cells proliferate and s/c cytokines (e.g. IFN-gamma, IL-2)
What is the typical histological appearance of a delayed-type hypersensitivity reaction?
proliferation of lymphocytes, monocytes, neutrophils, w/accumulations around small vessels (called "cuffing"), w/induration (hardening) due to fibrin formation
What are some examples of delayed-type hypersensitivity reactions?
tuberculin reaction, contact dermatitis (from delayed-hypersensitivity or direct chemical injury to skin)
What is the mechanism of CTL-mediated cytotoxicity?
sensitized CD8 T cells directly kill target cells w/antigen presented by self MHC class I (typically tumor or virus-infected cells)

(kill using perforin or Fas/apoptosis pathway)
What happens during hyperacute rejection?
antibody-mediated; preformed antibodies react immediately w/donor antigen and localized Arthus reaction follows (acute inflam, fibrinoid necrosis of small vessels, thrombosis)
What happens during acute cellular rejection?
days to months later; T-cell mediated, w/infiltration of lymphocytes and macrophages; if no arteritis, can respond promptly to immunosuppressants
What happens during acute humoral rejection (rejection vasculitis)?
antibody-mediated mechanisms cause vascular damage due to deposition of Ig's and complement, w/thrombosis and cortical necrosis
What happens during chronic rejection?
antibody-mediated vascular damage (vascular fibrointimal prolif), causes tubular atrophy and kidney shrinkage;

occurs months to years later; presents w/rise in serum creatinine over past 4-6mo
What is graft vs. host disease?
donor's T/B cells react a/g "foreign" host cells; CD8 cells damage directly, CD4 cells recruit macrophages, which damage host
In what clinical scenarios is graft vs host disease commonly seen?
-bone marrow transplantation (of immunocompetent cells),
-whole blood transfusion in patients with SCID
What are the principal target organs of graft-versus-host disease?
liver, skin, GI mucosa
What are the common presenting sx of graft-versus-host disease?
fever, rash, hepatosplenomegaly
Which types of sensitivity reactions involve complement?
Which types of sensitivity reactions are antibody mediated?
What are the common manifestations of type IV sensitivity reactions?
**4 T's**
T lymphocytes, Transplant rejections, TB skin tests, Touching (contact dermatitis)
What is the pneumonic for hypersensitivity reactions I through IV?
ACID: Anaphylactic and Atopic (I), Cytotoxic (II), Immune complex (III), Delayed (cell-mediated) (IV)