Type II hypersensitivity reaction

Figure 6.32 The basis of type II hypersensitivity reactions. The antigen is part of a cell, which becomes the target for macrophages, NK cells, neutrophils, and complement. Abbreviation NK, natural killer.

Immune-mediated reactions to penicillin G include anaphylaxis (a type 1 hypersensitivity reaction), hemolytic anemia and thrombocytopenia (type II hypersensitivity reactions). Anaphylactic reactions can be fatal, so epinephrine... 

Hypersensitivity can be defined as an exaggerated response of the immune system leading to host tissue damage. However, some of the immune responses described in the hypersensitivity classification below are, in some circumstances, appropriate responses to invading antigen. For example, a component in what is an appropriate immune response to tissue transplant rejection can be defined as a type II hypersensitivity reaction. 

As well as erythrocytes, other cells including platelets (thrombocytes) and some hanatopoietic precursor cells can be affected by drag-induced type II hypersensitivity reactions. Drag-induced thrombocytopenia for example is increasing as more drags are released and used. A number of different mechanisms appear to be involved. Drugs may bind covalently to the platelet mem-... 

Type II hypersensitivity results from the formation of antigen-antibody complexes between foreign antigen and IgM or IgG immunoglobulins. One example of this type of hypersensitivity is a blood transfusion reaction that can occur if blood is not cross-matched properly. Preformed antibodies bind to red blood cell membrane antigens that activate the complement cascade, generating a membrane attack complex that destroys the transfused red blood cells. In hemolytic disease of the newborn, anti-Rh IgG antibodies produced by an Rh-negative mother cross the placenta, bind to red... 

Toluenediisocyanate Allergy (type I), hypersensitivity reactions (type II)... 

Unlike the other types of hypersensitivity caused by antibodies, namely types II and ni, only a proportion of the population, the so-called atopies, have a predisposition to developing a type 1 hypersensitivity reaction when exposed to the allergen in question. Atopy may have a genetic component but type 11 and III reactions like, for example, penicillin-induced hemolytic anemia and serum sickness, may occur in all individuals, and this may result without a prior sensitization phase. 

The reaction is generally a type fV hypersensitivity response involving CD4+ cells, CD8+ cytotoxic lymphocytes and NK, Kupffer, and dendritic cells. Type II hypersensitivities may also sometimes occur. Knowledge of mechanisms underlying idiosyncratic drug-induced liver injury is limited. 

There are four main types of hypersensitivity reactions type I, II, and III hypersensitivity reactions are associated with the production of antibodies while type IV is cell mediated. Immediate hypersensitivity (type I) is due to IgE elicited by the antigen that binds to Fee receptor of mast cells or eosinophils, leading to their activation. Asthma due to platinum salts might be due to specific IgEs that have been found in sensitized patients. In addition, it seems that this agent triggers IgE production in rats (Pepys 1983). However, to our knowledge, this model has not been extensively studied. Type IV or delayed type hypersensitivity (DTH) is probably due to THl cells and is probably frequently involved in metal-mediated adverse side reactions. 

Immunologic Skin testing of 26 patients clinically diagnosed with immediate (type I) hypersensitivity to infliximab found seven positives (30%) and six of these had infliximab-reactive serum IgE antibo es. One skin test-positive patient had no detectable IgE antibodies to the mAb [155 ]. After multiple infusions with infliximab, a 61-year-old woman with Crohn s disease experienced an acute anaphylactic reaction immediately after the start of an infusion. Although anti-infliximab IgE antibodies were not detected, the concentration of anti-infliximab IgG was high and this remained the case 1 year after the mAb was discontinued. Substitution of adalimumab for infliximab 1 week after the anaphylactic reaction was tolerated until the 12th day when the patient displayed a delayed, type IV hypersensitivity reaction mediated by IgG antibodies specific for adalimumab [ISb ]. In addition to types I and IV hypersensitivities to infliximab, other immune-mediated reactions representing the other hypersensitivity states also occur to infliximab. This is illustrated by a recent report of a case of a 27-year-old woman of infliximab-induced systemic lupus erythematosus [157 ], an autoimmune connective tissue disease which is both a type II and a type III hypersensitivity response. 

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