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IL‐4 and IL‐10 Synergize to Suppress Mast Cell Development and IgE Receptor Expression
Author(s) -
Kolawole Motunrayo,
Speiran Kelly,
Bailey Daniel,
Ryan John
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.1075.16
Subject(s) - immunoglobulin e , interleukin 33 , mast cell , histamine , progenitor cell , cytokine , receptor , stem cell factor , biology , immunology , interleukin 5 , microbiology and biotechnology , interleukin 4 , interleukin , stem cell , antibody , endocrinology , biochemistry
IL‐4 and IL‐10 are co‐expressed by Th2 cells and have the potential to regulate the mast cell allergic response. One means by which mast cell homeostasis can be regulated is at the level of progenitor development. We have previously found that IL‐4 or IL‐10 can induce apoptosis in developing mouse mast cells. In the current study we demonstrate that these cytokines have synergistic activity, potently killing developing mast cells. Both cytokines also reduced IgE receptor expression on developing mast cells, and suppressed IgE‐mediated cytokine production or histamine release. The related cytokines IL‐13 and IL‐22 had similar activities, though generally less potent than IL‐4 or IL‐10. Lastly, we found that endogenous IL‐4 and IL‐10 may regulate mast cell development, since bone marrow from either IL‐4‐deficient or IL‐10‐deficient mice yielded mast cells with higher IgE receptor expression levels than their wild type counterparts. Our data demonstrate that IL‐4 and IL‐10 control mast cell homeostasis in part by regulating progenitor survival and IgE receptor expression. Supported by NIH grant 1R01 AI59638.