Cellular antimicrobial immunity.
Acquired resistance to infectious disease may be expressed by a predominantly humoral or a cellular mechanism or, more frequently, by a combination of the two. The cellular interactions which are responsible for the induction of the immune response in the skin, lung, intestinal mucosa, genitourinary tract, conjunctiva, and peritoneal cavity are discussed and the role of living or dead vaccines in the induction of acquired resistance is outlined. The host response involves three different cell types: the phagocytic cell (polymorphs or macrophages), the thymus-dependent (T) lymphocyte, and the thymus-independent (B) lymphocyte-plasma cell line. The normal unstimulated phagocytic cell is capable of killing most nonpathogenic bacteria that gain entry to the tissues. However, the presence of opsonic antibodies and activated macrophages is required to eliminate the pathogenic intracellular parasites. Such immunological activation involves the presence of sensitized T-lymphocytes in the lesion. The cellular response is also characterized by the simultaneous development of a state of delayed-type hypersensitivity (DTH), along with the antimicrobial CMI response. A rising humoral response normally develops subsequently. Killed bacterial cells (except when incorporated into Freund's complete adjuvant) induce the humoral response without the CMI reaction so that such vaccines are not able to fully protect the host against the naturally acquired disease. With the development of cell fractionation methods as well as the identification of distinctive cell surface markers, suspensions of B- and T-cells and macrophages can now be prepared for use in increasingly sophisticated transfer and reconstitution studies. The role of the different cell types in the expression of humoral and cellular immunity has been determined, and the effect of various immunopotentiating and immunosuppressive regimens on the immune system as a whole has been evaluated quantitatively. These studies have led to an appreciation of the role played by suppressor B- and T-cells in the interplay of both humoral and cellular components of the host defense system during the development of immune tolerance, desensitization, anergy, autoimmunity, and the expression of an anamnestic immune response following reinfection.
D000276:Adjuvants, Immunologic; D000818:Animals; D000917:Antibody Formation; D001402:B-Lymphocytes / Q000276:immunology; D001500:BCG Vaccine; D001419:Bacteria / Q000472:pathogenicity; D003228:Conjunctiva / Q000276:immunology; D004817:Epidermis / Q000276:immunology; D006801:Humans; D006968:Hypersensitivity, Delayed; D007111:Immunity, Cellular; D007112:Immunity, Maternally-Acquired; D007156:Immunologic Memory; D007165:Immunosuppression Therapy; D007239:Infections / Q000276:immunology* / Q000382:microbiology; D007422:Intestines / Q000276:immunology; D008168:Lung / Q000276:immunology; D008264:Macrophages / Q000276:immunology; D051379:Mice; D009504:Neutrophils / Q000276:immunology; D010529:Peritoneal Cavity / Q000276:immunology; D012485:Salmonella typhi / Q000472:pathogenicity; D013601:T-Lymphocytes / Q000276:immunology; D014566:Urogenital System / Q000276:immunology; D014774:Virulence
D000276:Adjuvants, Immunologic; D001500:BCG Vaccine