Genetic studies have shown an association between multiple autoimmune diseases and

TNFAIP3 (A20) and TNIP1 (ABIN1), both repressors of NF-B and of IKBKE (IKK epsilon), which is an NF-B activator. The aim of this study was to analyse single nucleotide polymorphisms (SNPs) in the IKBKE, NFKB1, TNIP1 and TNFAIP3 genes for association with primary SS. A total of 12 SNPs were genotyped in 1105 patients from Scandinavia (Sweden and Norway, n=684) and the UK (n=421) and 4460 controls (Scandinavia, n=1662, UK, n=2798). When patients were stratified for the presence of anti-SSA and/or anti-SSB antibodies (n=868), case-control meta-analysis found an association between antibody-positive primary SS and two SNPs in TNIP1 (P=3.4×10(-5), OR=1.33, 95%CI: 1.16-1.52 for rs3792783 and P=1.3×10(-3), OR=1.21, 95%CI: 1.08-1.36 for rs7708392). DMXAA concentration A TNIP1 risk haplotype was associated with antibody-positive primary SS (P=5.7×10(-3), OR=1.47, 95%CI: 1.12-1.92). There were no significant associations with IKBKE, NFKB1 or

TNFAIP3 in the meta-analysis of the Scandinavian and UK cohorts. We conclude that polymorphisms in TNIP1 are associated with antibody-positive primary SS.”
“Current theories of multiple sclerosis (MS) induction and progression place autoreactive T cells in the focus of the pathogenesis. Mesenchymal/stromal stem cells (MSC) have become a promising alternative approach for pathogenic therapy of MS due to their immunomodulatory properties, underlying mechanisms of which are intensive Selleck Lonafarnib study. Inositol monophosphatase 1 The objective

of the research was to investigate the contribution of PGE(2) to MSC-mediated suppression in patients with MS using in vitro model of mitogen- and myelin-stimulated T cell cocultivation with autologous/allogeneic MSC. We have showed that PGE(2) production depends on cell-to-cell contact of MSC and lymphocytes. The antigenic stimulation did not affect PGE(2) production following cocultivation of MSC and PBMC, and it is the presence of MSC in cell culture that significantly increases PGE(2) production irrespective of antigenic cultivation conditions. Simultaneously, PGE(2) synthesis correlated with indexes of MSC-mediated suppression of mitogen- and myelin-stimulated T cell proliferation in patients with MS. No significant differences in PGE(2) production by autologous and allogeneic MSC have been established. These results have demonstrated that in patients with MS, PGE(2) is one of the possible factors of MSC immunosuppression. The interrelation between PGE(2) concentrations and T cell proliferation suppression mediated by MSC may explain one of the immune mechanisms of cell therapy, which is crucial for the further proper use of MSC in MS research and pathogenic treatment.”
“In this study, we report the clinical and genetic features of Chinese patients with X-linked lymphoproliferative syndrome (XLP).