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The Role of Interleukin-10 (IL-10) in IL-15-Mediated T-Cell Responses
Dieter Körholz,
Ursula Banning,
Halvard Bönig,
Markus Grewe,
Marion Schneider,
Christine Mauz-Körholz,
Anne Klein-Vehne,
Jean Krutmann, and
Stephan Burdach
From the Departments of Pediatric Hematology and Oncology and Dermatology, Laboratory of Immunology, the Department of Transfusion Medicine and Hemostaseology, Heinrich-Heine University Medical Center, Biomedical Research Center Heinrich-Heine University, Düsseldorf, Germany.
Interleukin-15 (IL-15) is a potent T-cell stimulating factor, which has recently been used for pre-clinical in vivo immunotherapy. Here, the IL-15 effect on CD3-stimulated peripheral human T cells was investigated. IL-15 induced a significant T-cell proliferation and upregulated CD25 expression. IL-15 significantly enhanced T-cell production of interferon- (IFN-), tumor necrosis factor- (TNF-), and IL-10. Between 10- and 100-fold greater concentrations of IL-15 were necessary to reach a biological effect equivalent to that of IL-2. Blockade of IL-2 binding to the high-affinity IL-2 receptor did not affect the IL-15 effects, suggesting that IL-15 did not act by inducing endogenous IL-2. Exogenously administered IL-10 significantly reduced the IL-15 and IL-2-mediated IFN- and TNF- production, whereas T-cell proliferation and CD25 expression were not affected. The inhibitory effects of exogenously administered IL-10 on T-cell cytokine production appeared indirect, and are likely secondary to decreased IL-12 production by accessory cells. Inhibition of endogenous IL-10 binding to the IL-10 receptor significantly increased IFN- and TNF- release from T cells. These data suggest that endogenous IL-10 can regulate activated T-cell production of IFN- and TNF- via a paracrine negative feedback loop. The observations of this study could be of relevance for the therapeutic use of IL-15 in vivo.
Blood, Vol. 90 No. 11 (December 1), 1997:
pp. 4513-4521
© 1997 by The American Society of Hematology.
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