Abstract
Abstract [Purpose] Pathogen infection induces a shift to Th1 and inhibits a shift to Th2. The transcription factor IRF-1 is known to be essential for inducing IL-12 production and a shift to Th1. However, IRF-1 deficient cells express IL-12 p40 gene and induce Th1 cells during Listeria monocytogenes (Lm) infection. On the other hand, the effect of IRF-1 on Th2 is unknown. Since there is no inhibition of IL-4 production in the absence of IRF-1, we investigated the role of IRF-1 on IL-4 transcription during Lm infection. [Results] (1) IL-4 production of cloned Th2 (MS-SB) cells was not inhibited by Lm infection of the clone. (2) When the mixture of MS-SB and T-depleted wild type or IRF-1 KO splenic cells were infected with Lm, Il-4 production was inhibited. Therefore, IRF-1 functions to inhibit IL-4 production in Th2 cells. (3) We transfected MS-SB cells with Luciferase reporter plasmid containing IL-4 promoter and IRF-1 expression plasmid. When MS-SB cells were stimulated with PMA plus Ionomycin, IL-4 production was inhibited without affecting Luciferase activity. Therefore, IRF-1 does not inhibit IL-4 promoter activity. [Conclusion] There are two silencer regions in down stream of IL-4 coding region, and these silencers contain IRF-1 binding motif. Our results suggest that IRF-1 functions as a negative regulator for IL-4 gene transcription via silencer regions in Th2 cells during Lm infection.
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