[ $TGF-{eta}1$ ]is well known to induce Ig germ-line ${alpha}$ ($GL{alpha}$) transcription and subsequent IgA isotype class switching recombination (CSR). Homeodomain protein TG-interacting factor (TGIF) and E3-ubiquitin ligases TGIF interacting ubiquitin ligase 1 (Tiul1) are implicated in the negative regulation of $TGF-{eta}$ signaling. In the present study, we investigated the roles of Tiul1 and TGIF in $TGF{eta}1$-induced IgA CSR. We found that over-expression of Tiul1 decreased $TGF{eta}1$-induced $GL{alpha}$ promoter activity and strengthened the inhibitory effect of Smad7 on the promoter activity. Likewise, overexpression of TGIF also diminished $GL{alpha}$ promoter activity and further strengthened the inhibitory effect of Tiul1, suggesting that Tiul1 and TGIF can down-regulate $TGF{eta}1$-induced $GL{alpha}$ expression. In parallel, overexpression of Tiul1 decreased the expression of endogenous IgA CSR-predicitive transcripts ($GLT_{alpha},;PST_{alpha},;and;CT_{alpha}$) and $TGF{eta}1$-induced IgA secretion, but not $GLT_{gamma3}$ and IgG3 secretion. Here, over-expressed TGIF further strengthened the inhibitory effect of Tiul1. These results suggest that Tiul1 and TGIF act as negatively regulators in $TGF{eta}1$-induced IgA isotype expression.