TGF-β1 enhances mouse mast cell release of IL-6 and IL-13

Abstract

For immune cells, TGF-{beta}1 can enhance or repress effector functions. Here, we characterize the effects of TGF-{beta}1 on IgE-mediated activation of primary murine mast cells derived from hematopoietic stem cells (BMMC). We also investigated potential interaction between TGF-{beta}1 and stem-cell factor (SCF). Resting IL-6 production was increased with TGF-{beta}1 but significance was lost following BMMC activation via IgE receptor (Fc{varepsilon}RI) crosslinking. SCF also enhanced resting levels of IL-6, but there was no difference from control once Fc{varepsilon}RI was engaged. SCF had no effect on IL-13 production; however, TGF-{beta}1 treatment enhanced release of IL-13 upon Fc{varepsilon}RI activation. Lastly, percent colocalization of SCF receptor (CD117) and Fc{varepsilon}RI were unaffected by TGF-{beta}1 treatment. These data reveal a novel positive effect of soluble TGF-{beta}1 on mast cell activation.