Type I reactions
Type I hypersensitivity reactions are rapid and short-lived anaphylactic reactions that do not cause chronic tissue injury. Prior antigenic exposure to certain antigens leads to IgE synthesis, which serves as antigen receptor on the surface of mast cells. Binding of antigen to IgE triggers mast cell degranulation, releasing histamine and other acute inflammatory mediators. For example, hydatid cyst rupture can cause anaphylaxis.
Type II reactions
Tissue damage associated with type II hypersensitivity reactions are mediated by antibodies to microbial antigens that cross react with host cell antigens.For example,certain M serotypes of the Lancefield group A Streptococcus pyogenes stimulate high titres of immunoglobulin G (IgG) that cross-react with host cell antigens in the heart,joints and neural tissue, leading to the carditis, arthritis and Sydenham’schorea,whch characterize rheumatic fever.
Type III reactions
Type III hypersensitivity reactions to infectious diseases are also mediated by antibodies.Immune complex formation between antigens and antibodies results in activation of complement and chemotaxis of neutrophils that release tissue-damaging enzymes. Aggregation of platelets also causes formation of micro-thrombi and release of vasoactive amines. Many different tissues may be affected and polymorphonuclear infiltration, oedema and vasculitis characterize lesions. The natural history of such reactions is commonly persistent and chronic. Examples include glomerulonephritis associated with bacterial endocarditis, erythema nodosum leprosum (a hypersensitivity reaction to persistent M. leprae antigens in the skin) and allergic bronchopulmonary aspergillosis (which causes pulmonary infiltration and airflow obstruction in response to Aspergillus fumigatus.
Type IV reactions
Type IV reactions cause cell-mediated tissue pathology in which there is delayed-type hypersensitivity (DTH).The accumulation of large numbers of highly activated macrophages and formation of granulomas characterize tissue lesions. This is the classical mechanism by which the host response may cause very extensive and chronic tissue damage. Examples include TB, tuberculoid leprosy and periportal hepatic fibrosis in Schistosoma mansoni infection.
