| First Author | Kennedy Norton S | Year | 2008 |
| Journal | J Immunol | Volume | 180 |
| Issue | 5 | Pages | 2848-54 |
| PubMed ID | 18292506 | Mgi Jnum | J:131544 |
| Mgi Id | MGI:3773947 | Doi | 10.4049/jimmunol.180.5.2848 |
| Citation | Kennedy Norton S, et al. (2008) IL-10 Suppresses Mast Cell IgE Receptor Expression and Signaling In Vitro and In Vivo. J Immunol 180(5):2848-54 |
| abstractText | Mast cells are known for their roles in allergy, asthma, systemic anaphylaxis, and inflammatory disease. IL-10 can regulate inflammatory responses and may serve as a natural regulator of mast cell function. We examined the effects of IL-10 on in vitro-cultured mouse and human mast cells, and evaluated the effects of IL-10 on FcepsilonRI in vivo using mouse models. IgE receptor signaling events were also assessed in the presence or absence of IL-10. IL-10 inhibited mouse mast cell FcepsilonRI expression in vitro through a Stat3-dependent process. This down-regulation was consistent in mice tested in vivo, and also on cultured human mast cells. IL-10 diminished expression of the signaling molecules Syk, Fyn, Akt, and Stat5, which could explain its ability to inhibit IgE-mediated activation. Studies of passive systemic anaphylaxis in IL-10-transgenic mice showed that IL-10 overexpression reduced the IgE-mediated anaphylactic response. These data suggest an important regulatory role for IL-10 in dampening mast cell FcepsilonRI expression and function. IL-10 may hence serve as a mediator of mast cell homeostasis, preventing excessive activation and the development of chronic inflammation. |
