Hypersensitivity Reactions Questions and Answers

Answer: B

The cause is that complement is activated and membrane attack complex lyse RBCs.

In autoimmune haemolytic anaemia (the paper's 'autonomic' hemolysis), autoantibodies bind antigens on the patient's own red cells. Bound antibody, especially IgM, activates the classical complement pathway; the terminal components C5b to C9 assemble the membrane attack complex, which punches pores in the red cell membrane and lyses it. Antibody- and C3b-coated cells are also cleared by phagocytes in the spleen and liver.

Granzymes are released by cytotoxic T cells and NK cells, not neutrophils. Red cells carry no MHC class I, so cytotoxic T cells do not lyse them, and red cells have no IL-2 receptor.

Answer: D

The immunoglobulin is IgE.

IgE binds through its Fc region to high-affinity FcεRI receptors on mast cells and basophils. When an allergen cross-links the bound IgE, these cells degranulate and release histamine, leukotrienes and other mediators. This is type I (immediate) hypersensitivity, the mechanism behind hay fever, allergic asthma and anaphylaxis.

IgA is the main antibody of mucosal secretions and breast milk. IgM is the first antibody made in a primary response and forms pentamers. IgD sits mainly on the surface of naive B cells as an antigen receptor. None of them drives allergy and asthma the way IgE does.