Pathologic concentrations of interleukin 6 inhibit T cell responses via induction of activation of TGF-beta.
Interleukin 6 levels are increased in a variety of clinical conditions including bacterial and viral infections, HIV infection, autoimmune diseases, certain neoplasias, and traumatic injury. In general, all these conditions are characterized by suppression of one or more manifestations of the immune response. Concentrations of IL 6 comparable to those found in the sera of immunosuppressed, thermally injured patients selectively inhibit T cell proliferative responses. This suppression is independent of IL 2-mediated responses, is dependent on macrophage activity, and is reversed by antisera specific for transforming growth factor-beta (TGF-beta).
Zhou
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Department of Surgery, Johns Hopkins University School of Medicine, Baltimore, Maryland 21224.
Munster
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Winchurch
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RA
D000818:Animals; D002455:Cell Division; D002478:Cells, Cultured; D003208:Concanavalin A / Q000494:pharmacology; D007376:Interleukin-2 / Q000032:analysis; D015850:Interleukin-6 / Q000032:analysis / Q000494:pharmacology*; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D015375:Receptors, Interleukin-2 / Q000032:analysis; D013601:T-Lymphocytes / Q000187:drug effects / Q000276:immunology / Q000502:physiology*; D016212:Transforming Growth Factor beta / Q000378:metabolism*
D007376:Interleukin-2; D015850:Interleukin-6; D015375:Receptors, Interleukin-2; D016212:Transforming Growth Factor beta; D003208:Concanavalin A