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Insulin‐like growth factor‐I stimulates IL‐10 production in human T cells
Author(s) -
Kooijman Ron,
Coppens Astrid
Publication year - 2004
Publication title -
journal of leukocyte biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.819
H-Index - 191
eISSN - 1938-3673
pISSN - 0741-5400
DOI - 10.1189/jlb.0404248
Subject(s) - cytokine , biology , peripheral blood mononuclear cell , tumor necrosis factor alpha , secretion , immune system , monocyte , lipopolysaccharide , growth factor , insulin like growth factor , interleukin , interleukin 10 , endocrinology , immunology , medicine , in vitro , receptor , biochemistry
There is vast body of evidence that the insulin‐like growth factor (IGF)‐I exerts immunomodulatory effects in vitro and in vivo. In vitro studies indicate that stimulatory effects of IGF‐I may be exerted through augmentation of inflammatory cytokine production. To further explore the immunomodulatory effects of IGF‐I through regulation of cytokine production, we tested the in vitro effects of IGF‐I on the secretion of inflammatory T helper cell type 1 (Th1) and Th2 cytokines by human peripheral blood mononuclear cells (PBMC). To this end, PBMC were stimulated with the T cell mitogen phytohemagglutinin (PHA), and cytokines in the culture media were assessed after 18, 42, 66, and 80 h of culture. We found that IGF‐I stimulated the secretion of the Th2 cytokine interleukin (IL)‐10 by 40–70% in PHA‐stimulated PBMC. In addition, we observed a small stimulatory effect (15%) on the secretion of another Th2 cytokine IL‐4. The secretion of IL‐2, IL‐5, IL‐6, interferon‐γ, and the inflammatory cytokines IL‐1β, IL‐8, and tumor necrosis factor α was not or was hardly affected. IL‐10 secretion was also stimulated in purified T cells, and we established that IGF‐I also stimulated IL‐10 mRNA expression by 100–150%. The monocyte‐activating bacterial cell‐wall product lipopolysaccharide induced IL‐10 production in PBMC, but this was not affected by IGF‐I. As IL‐10 predominantly exerts anti‐inflammatory actions and suppresses Th1‐dependent immune responses, our results indicate that IGF‐I may exert inhibitory actions on inflammatory and Th1‐mediated cellular immune responses through stimulation of IL‐10 production in T cells.

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