Our results suggest that computerised teaching methods have significant potential to assist in learning for both Chinese and foreign medical undergraduates.

To investigate the effects of altered collagen II (CII) peptide ligands in collagen-induced arthritis (CIA), CIA rats were subcutaneously injected with an altered CII263-272 peptide ligand (APL, 100, 10, and 1 microg/dose, six dose each, twice a week), which had been identified by us as an inhibitory effect on CII-specific T-cell activation in vitro in rheumatoid arthritis (RA). Clinical, radiographic, and histologic scores were evaluated. Serum level of interferon (IFN)-gamma was assessed by enzyme-linked immunosorbent assay, and the numbers of interleukin (IL)-4-producing cells in vitro in memory responses to the APL were determined by enzyme-linked immunospot. The results showed significantly reduced arthritis scores in CIA rats treated with 100 microg/dose of APL compared with those treated with phosphate buffered solution (PBS) and control peptide. The mean radiographic and histologic scores were also markedly lower in APL-treated CIA rats. On day 35 after immunization, a significantly lower level of IFN-gamma in serum was found in APL-treated rats, accompanied by increased numbers of IL-4-producing cells, indicating that APL treatment skewed the T helper (Th)1/Th2 balance toward Th2-type response in vivo. Altered CII263-272 peptide ligand immunization induces inhibition of CIA through a shift toward Th2-type response, suggesting that altered CII peptide might be a potential therapeutic target for RA.

No abstract

Objectives The aim of our study was to elucidate whether umbilical cord derived mesenchymal stem cell (UC-MSCs) had immunomodulatory effect on T follicular helper (Tfh) cell under rheumatoid arthritis (RA) background. Methods PBMCs that isolated from RA patients and healthy contorl (HC) were cocultured with UC-MSCs at a ratio of 100:1, 10:1 and 1:1 respectively through cell-to-cell contact or in a transwell system at a ratio of 1:10. After 3 days' coculture, PBMCs were collected and the frequency of CD4+CXCR5+PD-1+T cell was examined by flow cytometry. Purified naïve T cells isolated from PBMC of RA patients were cocultured with human UC-MSCs for 4 days at a ratio of 1:10 under Tfh cell-polarizing condition. To detect the effect of MSC on Tfh proliferation, CFSE-labeled purified CD4+ T cells isolated from PBMC of RA patients or HC were stimulated with anti-CD3/CD28 and cocultured with UC-MSCs for 5 days. The frequency of CD4+CXCR5+PD-1+T or CD4+CXCR5+PD-1+AnnexinV+T was examined by flow cytometry and the level of IL-21 in the cultured supernatant was measured by ELISA. The mRNA levels of indoleamine 2,3-dioxygenase (IDO), IL-10, PGE2, HGF, TGF-β and HLA-G in UC-MSCs were tested by RT-PCR. IDO activity of was measured by high-performance liquid chromatography (HPLC), and P-STAT-1/3/5 and p-Akt in UC-MSCs were tested by Western blot. IDO inhibitor 1-MT or anti-IL-10 antibody was added into UC-MSCs and Tfh cell differentiation coculture system for 5 days and then the frequency of CD4+CXCR5+PD-1+T was examined by flow cytometry. Results UC-MSCs were able to suppress the generation of Tfh cell both in RA patients and in HC in vitro, which was dose-dependent and not relied on cell-to cell contact. UC-MSCs suppressed the differentiation and proliferation of Tfh cell that was more prominent in samples from RA patients, but had no effect on Tfh cell apoptosis. The level of IL-21 in UC-MSCs and Tfh cell differentiation coculture system was significantly decreased. Dramatic increases of both IDO mRNA expression and IDO enzymatic activity were detected in UC-MSCs after coculturing with naïve T cells under Tfh cell-polarizing condition. Meanwhile, pSTAT-1/3/5 and pAkt in these UC-MSCs were increased. The addition of the IDO inhibitor 1-MT, but not anti-IL-10 antibody, could reverse the suppressive effect of UC-MSCs on the differentiation of Tfh cell. Conclusions UC-MSCs suppress Tfh cell differentiation and proliferation in RA patients, which is partially mediated by the secretion of IDO. Disclosure of Interest None declared DOI 10.1136/annrheumdis-2014-eular.2202