CD26 (DPPIV) recently was demonstrated directly involved in regulating IP-10 activity by NH2-terminal truncation. Lower sCD26 was associated with favorable treatment outcome of chronic hepatitis C. We hypothesized that vitamin D supplement, which was shown to improve CHC treatment response, might act upon restoring immune dysregulation in these patients through a pathway linked to the Th1/Th2 cytokines, IP-10 or CD26. METHODS: CHC patients with vitamin D deficiency were assigned to receive vitamin D supplement or placebo for 6 weeks. Baseline characteristics, serum 25-hydroxy vitamin D [25(OH)D] levels, Th1/Th2

cytokines, IP-10 and sCD26 levels were measured at baseline and at 6 weeks. SB203580 cost RESULTS: A total of 80 CHC patients with vitamin Metabolism inhibitor D deficiency were randomized into two groups, 40 patients in each group. There were no significant differences in all baseline characteristics between two groups. At the end of study, only the mean 25(OH)D levels in vitamin D group were significantly increased from 21.07 to 48.44 ng/ml, (p<0.001). There were no significant differences in serum levels of all Th1/Th2 cytokines in both groups at the end of the study period. Importantly, while there were no significant changes of the IP-1 0 and sCD26 levels in placebo group, there were significant

decreased in serum levels of both chemokines in vitamin D group after 6-week of vitamin D supplement (p<0.05 and p<0.05, respectively) (Fig.1). CONCLUSIONS: Correction of vitamin D deficiency in CHC patients resulted in suppression of serum IP-1 0 and sCD26 levels without the effect on serum Th1/Th2 cytokines.These results, at least, identified an immuno-pathophysiologic

link between an important chemo-tactic chemokine with its regulating molecule (sCD26) and effects of vitamin D replacement therapy, and provided an explanation of why vitamin D deficiency might have an effect on CHC treatment responses. Disclosures: The following people have nothing to disclose: Kriangsak Charoensuk, Chintana Chirathaworn, Sirinporn Suksawatamnuay, Panarat Thaimai, Kessarin Thanapirom, Kittiyod Poovorawan, Pinit Kullavanijaya, Piyawat Komolmit Objective: Methane monooxygenase Persistent hepatitis C virus (HCV) infection causes not only liver disease but also extrahepatic effects, such as type 2 diabetes. Patients with chronic hepatitis C (CHC) complicated by type 2 diabetes show resistance to interferon (IFN) therapy. Selenoprotein P (SeP), a liver-derived secretory protein, causes insulin resistance and plays an important role in the pathogen-esis of type 2 diabetes (Cell Metab. 201 0); however, its effects on IFN signaling have not been clarified. Methods: SeP gene expression was suppressed in Huh-7.