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Type II hypersensitivity: Wikis


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From Wikipedia, the free encyclopedia

Hypersensitivity types
Type I - Allergy (immediate)
Type II - Cytotoxic, antibody-dependent
Type III - Immune complex disease
Type IV - Delayed-type hypersensitivity
(Antibody Independant)
Type V - Autoimmune disease
Type II hypersensitivity
Classification and external resources
DiseasesDB 33482
MedlinePlus 000821
MeSH D001327

In type II hypersensitivity (or cytotoxic hypersensitivity)[1 ] the antibodies produced by the immune response bind to antigens on the patient's own cell surfaces. The antigens recognized in this way may either be intrinsic ("self" antigen, innately part of the patient's cells) or extrinsic (absorbed onto the cells during exposure to some foreign antigen, possibly as part of infection with a pathogen). These cells are recognized by macrophages or dendritic cells which act as antigen presenting cells, this causes a B cell response where antibodies are produced against the foreign antigen.

An example here is the reaction to penicillin where the drug can bind to red blood cells causing them to be recognised as different, B cell proliferation will take place and antibodies to the drug are produced. IgG and IgM antibodies bind to these antigens to form complexes that activate the classical pathway of complement activation to eliminate cells presenting foreign antigens (which are usually, but not in this case, pathogens). That is, mediators of acute inflammation are generated at the site and membrane attack complexes cause cell lysis and death. The reaction takes hours to a day.

Another form of type II hypersensitivity is called antibody-dependent cell-mediated cytotoxicity (ADCC). Here, cells exhibiting the foreign antigen are tagged with antibodies (IgG or IgM). These tagged cells are then recognised by natural killer (NK) cells and macrophages (recognised via IgG bound (via the Fc region) to the effector cell surface receptor, CD16 (FcγRIII)), which in turn kill these tagged cells.

Some examples

Disease Target antigen Pathophysiology Main effects
Autoimmune hemolytic anemia Rh antigens, I antigen on RBCs Opsonization and phagocytosis of erythrocytes
Hemolytic disease of the newborn (HDN) *
(erythroblastosis fetalis)
Antigens on erythrocytes RBS degradation
Autoimmune thrombocytopenic purpura Glycoprotein IIb/IIIa on platelets Opsonization and phagocytosis of platelets Bleeding diathesis
Pemphigus vulgaris Epidermal cadherins
ANCA-associated vasculitides Neutrophil granule proteins Neutrophil degranulation and inflammation
  • Vasculitis
Goodpasture's syndrome Noncollagenous protein Complement and Fc-receptor-mediated inflammation
Acute rheumatic fever M proteins on Group A streptococci and then myocardial antigen
  • Macrophage activation
  • Inflammation
  • Myocarditis
  • Arthritis
Myasthenia gravis Acetylcholine receptor Competitive acetylcholine inhibition
Receptor down-regulation
  • Muscle weakness
  • Paralysis
Graves disease TSH receptor Receptor agonism
Pernicious anemia (if autoimmune) Intrinsic factor on gastric parietal cells Decreased vitamin B12 absorption
  • Abnormal erythropoiesis
  • Anemia
Unless else specified in boxes, then ref is: [2]

* - HDN not taken from [2]

Other examples are:


  1. ^ "Hypersensitivity reactions".  
  2. ^ a b Table 5-3 in: Mitchell, Richard Sheppard; Kumar, Vinay; Abbas, Abul K.; Fausto, Nelson. Robbins Basic Pathology. Philadelphia: Saunders. ISBN 1-4160-2973-7.   8th edition.


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