| First Author | Ndaw VS | Year | 2017 |
| Journal | J Immunol | Volume | 199 |
| Issue | 3 | Pages | 866-873 |
| PubMed ID | 28637902 | Mgi Jnum | J:251445 |
| Mgi Id | MGI:6099425 | Doi | 10.4049/jimmunol.1601983 |
| Citation | Ndaw VS, et al. (2017) TGF-beta1 Suppresses IL-33-Induced Mast Cell Function. J Immunol 199(3):866-873 |
| abstractText | TGF-beta1 is involved in many pathological conditions, including autoimmune disorders, cancer, and cardiovascular and allergic diseases. We have previously found that TGF-beta1 can suppress IgE-mediated mast cell activation of human and mouse mast cells. IL-33 is a member of the IL-1 family capable of inducing mast cell responses and enhancing IgE-mediated activation. In this study, we investigated the effects of TGF-beta on IL-33-mediated mast cell activation. Bone marrow-derived mast cells cultured in TGF-beta1, beta2, or beta3 showed reduced IL-33-mediated production of TNF, IL-6, IL-13, and MCP-1 in a concentration-dependent manner. TGF-beta1 inhibited IL-33-mediated Akt and ERK phosphorylation as well as NF-kappaB- and AP-1-mediated transcription. These effects were functionally important, as TGF-beta1 injection suppressed IL-33-induced systemic cytokines in vivo and inhibited IL-33-mediated cytokine release from human mast cells. TGF-beta1 also suppressed the combined effects of IL-33 and IgE-mediated activation on mouse and human mast cells. The role of IL-33 in the pathogenesis of allergic diseases is incompletely understood. These findings, consistent with our previously reported effects of TGF-beta1 on IgE-mediated activation, demonstrate that TGF-beta1 can provide broad inhibitory signals to activated mast cells. |
