Abstract
Mast cell activation is associated with atopic and inflammatory diseases. Despite this, the natural controls of mast cell homeostasis are poorly understood. We have found that ILā10 and TGFb1 suppress mast cell function and have investigated how these cytokines might be available to mast cells during the inflammatory response. Regulatory T cells (Treg) are a subāclass of CD4+ T cells that can produce both ILā10 and TGFb1. We hypothesized that these cells could function in mast cell homeostasis. In this study, we demonstrate that mast cells can recruit Treg. Furthermore, Treg, but not CD4+/CD25ā T cells, suppress mast cell FceRI expression. Despite the inhibitory effects of ILā10 and TGFb1, Treg effects were independent of ILā10 and TGFāb1, and required cell contact. Surprisingly, coāculture with either Treg or CD25ā T cells enhanced IgEāmediated cytokine production by mast cells. These data are the first demonstration that mast cells can recruit Treg and that these interactions may alter the mast cell response. Supported by NIH grant 1R01 AI59638.
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