IFN-γ Induces Apoptosis in Developing Mast Cells

摘要: Mast cells are critical effectors of allergic disease, and now implicated in immune responses observed arthritis, multiple sclerosis, heart disease. Because their role inflammation, understanding how mast develop is clinical importance. In this study we determined the effects IFN-gamma on cell survival. Using vitro culture bone marrow IL-3 plus stem factor, found that addition induced apoptosis, as exhibited by presence subdiploid DNA caspase activation. IFN-gamma-mediated apoptosis was Stat1-dependent, accompanied loss mitochondrial membrane potential. Apoptosis reduced cultures derived from p53- or Bax-deficient mice, well H2K-Bcl-2 transgenic mice. hyperresponsiveness has been shown to result inflammatory disease death mice lacking regulatory protein suppressor cytokine signaling (SOCS)-1. Bone SOCS-1 knockout (KO) failed give rise viable after with profound occurring matured. However, both survived normally. This defect development recapitulated vivo. KO demonstrated a 67% decrease peritoneal numbers relative wild-type deficiency reversed SOCS-1/IFN-gamma These data demonstrate potent survival show can elicit