Regulation of lymphokine function.
Although we have focused on desensitization as an experimental model, the findings obtained suggest mechanisms by which physiological control of cell-mediated immunity is attained. Thus, such regulation may occur either at the stage of expression of lymphokine activity or at the level of lymphokine production itself. The former may involve unique suppressor molecules, but as indicated above may be due to the inflammatory lymphokines themselves. The latter appears to involve suppressor systems similar to those operative in antibody formation. Over and above any specific model for regulation, the findings presented here suggest that local fluctuations in lymphokine distribution can modulate immunologically induced inflammatory responses, either through alterations in chemotactic gradients, or by other mechanisms as yet unknown.
D000818:Animals; D001402:B-Lymphocytes / Q000276:immunology; D002630:Chemotactic Factors; D003888:Desensitization, Immunologic; D006168:Guinea Pigs; D006968:Hypersensitivity, Delayed / Q000276:immunology; D007165:Immunosuppression Therapy; D007249:Inflammation / Q000276:immunology; D008214:Lymphocytes / Q000276:immunology; D008222:Lymphokines / Q000008:administration & dosage / Q000097:blood / Q000502:physiology*; D008263:Macrophage Migration-Inhibitory Factors / Q000494:pharmacology; D008264:Macrophages / Q000276:immunology; D013601:T-Lymphocytes / Q000276:immunology
D002630:Chemotactic Factors; D008222:Lymphokines; D008263:Macrophage Migration-Inhibitory Factors