1. Induction of IL-10 synthesis by human keratinocytes through CD23 ligation: a cyclic adenosine 3',5'-monophosphate-dependent mechanism.
- Author
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Bécherel PA, LeGoff L, Francès C, Chosidow O, Guillosson JJ, Debré P, Mossalayi MD, and Arock M
- Subjects
- Adjuvants, Immunologic physiology, Antibodies, Monoclonal, Cells, Cultured, Humans, Infant, Newborn, Interleukin-10 genetics, Interleukin-10 immunology, Nitric Oxide physiology, RNA, Messenger biosynthesis, Receptors, IgE immunology, Tumor Necrosis Factor-alpha biosynthesis, Cyclic AMP physiology, Interleukin-10 biosynthesis, Keratinocytes immunology, Keratinocytes metabolism, Receptors, IgE metabolism
- Abstract
Ligation of the low affinity receptor for IgE, CD23/Fc epsilonRII, in human keratinocytes (HK) and monocytes induces the synthesis of proinflammatory cytokines (IL-6 and TNF-alpha), partly under the dependence of cAMP and nitric oxide pathways. Moreover, CD23 ligation induces IL-10 production in human monocytes. Since synthesis of IL-10 by HK is still a matter of debate, we investigate whether keratinocytes could produce IL-10 upon CD23 stimulation. Here, our data show that CD23 ligation induces significant IL-10 synthesis in HK, a phenomenon inhibited by cAMP antagonists, but not by inhibitors of the nitric oxide pathway. Accordingly, cAMP agonist induced significant IL-10 synthesis by HK, while nitric oxide-releasing chemical did not. Treatment of HK with anti-IL-10 mAb potentiated their CD23-mediated TNF-alpha synthesis. These data indicate that engagement of surface CD23 on human keratinocytes induces the synthesis of IL-10, which, in turn, down-regulates their proinflammatory response.
- Published
- 1997