IFN-${gamma}$ has been shown to either up- or down-regulate the expression of specific TGF-${eta}$1-induced target genes. We investigated the effect of IFN-${gamma}$ on TGF-${eta}$1-induced IgA isotype expression. We found that IFN-${gamma}$ inhibited not only TGF-${eta}$1-induced germ-line (GL) ${alpha}$ transcription, but also IgA secretion by TGF-${eta}$1-stimulated murine B cells. Overexpression of Stat1 diminished TGF-${eta}$1-induced, Smad3/4- and Runx3-mediated GL${alpha}$ promoter activity. Overexpression of p300 also increased the promoter activity, while its effect was abrogated by co-transfected Stat1. Stat1 interfered with the Smad3:p300 interaction, likely due to a stronger Stat1:p300 binding affinity. These results indicate that Stat1 can inhibit GL${alpha}$ transcription through binding to p300. Further, overexpression of SOCS1, a JAK inhibitor, diminished the antagonistic effect of IFN-${gamma}$ on TGF-${eta}$1-induced GL${alpha}$ transcription and IgA secretion. These results indicate that JAK/Stat1-mediated IFN-${gamma}$ signaling antagonizes TGF-${eta}$1-induced GL${alpha}$ transcription, mainly through deprivation of p300 from Smad3, resulting in decreased IgA synthesis.