Role of cytokines in tuberculosis.
Mycobacterium tuberculosis and Mycobacterium bovis are facultative intracellular pathogens which preferentially utilize the macrophage as their host cell. Acquired resistance against mycobacteria depends on T cells which activate antimicrobial macrophage functions via the release of cytokines. The data summarized below suggest an important role for interferon-gamma (IFN-gamma) as well as the B cell-stimulatory factors interleukin-4 (IL-4) and IL-6 in the induction of tuberculostatic macrophage functions. Growth inhibition of mycobacteria by cytokine-stimulated macrophages is mediated by reactive nitrogen intermediates (RNI) derived from L-arginine. Tumor necrosis factor-alpha (TNF-alpha) and IL-10 act as autocrine regulators in the induction of the enzyme NO-synthase. Both cytokines are produced by macrophages stimulated with IFN-gamma and infected with M. bovis. While TNF-alpha mediates activation of the NO-synthase and production of RNI, IL-10 suppresses this enzyme activity. The outcome of mycobacterial infection is probably regulated by a complex network between stimulatory and inhibitory cytokines.
Flesch
I E
IE
Department of Immunology, University of Ulm, Germany.
Kaufmann
S H
SH
D000818:Animals; D016207:Cytokines / Q000502:physiology*; D006801:Humans; D008264:Macrophages / Q000201:enzymology / Q000276:immunology; D009169:Mycobacterium tuberculosis / Q000254:growth & development / Q000276:immunology; D010587:Phagocytosis / Q000502:physiology; D013601:T-Lymphocytes / Q000276:immunology; D014376:Tuberculosis / Q000276:immunology* / Q000382:microbiology
D016207:Cytokines