Immune responses in parasitic diseases. Part B: mechanisms.
A number of host defenses provide variable resistance against parasites. From the biological point of view, invading parasites must not eliminate the susceptible host population; therefore, antiparasite immunity plays an essential role in limiting the invasion and proliferation of parasites. Several differences exist between immune responses to parasites and immune responses to other microorganisms. Effector mechanisms include T lymphocyte-mediated inflammatory granuloma formation and encapsulation involving the deposition of fibrous tissue. In some instances, passive immunity can be transferred by serum antibodies. Antibodies may act via complement fixation, granulocyte adhesion, opsonization, inhibition of invasion, or mast cell degranulation. Of the nonspecific factors, macrophage activation, natural killer cells, and serum factors other than antibodies are critical in the battle against parasites. The net result of these immune responses may be antiparasitic, proparasitic, of no consequence to either host or parasite, or harmful to the host.
D000818:Animals; D000917:Antibody Formation; D003602:Cytotoxicity, Immunologic; D006373:Helminthiasis / Q000276:immunology; D006801:Humans; D007113:Immunity, Innate; D007116:Immunization, Passive; D007413:Intestinal Mucosa / Q000276:immunology; D007898:Leishmaniasis, Visceral / Q000276:immunology; D008264:Macrophages / Q000276:immunology; D051379:Mice; D010272:Parasitic Diseases / Q000276:immunology*; D051381:Rats; D012552:Schistosomiasis / Q000276:immunology; D013601:T-Lymphocytes / Q000276:immunology; D013622:Taeniasis / Q000276:immunology