Epigallocatechin-3-gallate maintains Th1/Th2 response balance and mitigates type-1 autoimmune diabetes induced by streptozotocin through promoting the effect of bone-marrow-derived mesenchymal stem cells.

Stem-cell-based therapy is one of the most promising therapeutic strategies owing to its regenerative and immunomodulatory properties. Epigallocatechin-3-gallate (EGCG), a known antioxidant and anti-inflammatory agent, has beneficial effects on cellular protection. We aimed to elucidate the feasibility of using EGCG, along with bone marrow-derived mesenchymal stem cells (BM-MSCs), to improve pancreatic damage through their immune regulatory functions in an experimental model of type 1 diabetes mellitus (T1DM) induced by multiple injections of streptozotocin (STZ). BM-MSCs were isolated from C57BL/6 mice and characterized. The diabetic groups were treated intraperitoneally with PBS, MSCs, EGCG, and a combination of MSCs and EGCG. Real-time PCR assays showed that MSCs with EGCG modulated T-bet and GATA-3 expression and upregulated the mRNA levels of Foxp-3 more efficiently. Analyses of spleen-isolated lymphocytes revealed that combinational treatment pronouncedly increased regulatory cytokines and decreased pro-inflammatory cytokines and splenocyte proliferation. The histopathological assessment demonstrated that co-treatment significantly reduced insulitis and recovered pancreatic islet morphology. Furthermore, the combination of MSCs and EGCG is associated with downregulated blood glucose and enhanced insulin levels. Therefore, combined therapy with EGCG and MSCs holds clinical potential for treating T1DM through synergetic effects in maintaining the Th1/Th2 response balance and promoting the regeneration of damaged pancreatic tissues.

Role of exosome in autoimmunity, with a particular emphasis on rheumatoid arthritis.

Cell-derived exosomes are identified as carriers of lipids, proteins, and genetic materials that participate in cell-cell signal communication, biological process, and cell signaling. Also, their involvement has been reported in a vast array of disorders and inflammatory conditions such as autoimmune diseases. Rheumatoid arthritis (RA), a common cause of joint disorder, is an inflammation-based disease in which the precise understanding of its pathogenesis needs to be further investigated. Also, there is only a palliative care approach for the alleviation of RA symptoms. This paper discusses the recent advances in the biology of exosomes in autoimmune disorders especially in RA, and also provides a new line of research for arthritis therapy using exosomes.

Neopterin serum level does not reflect the disease activity in rheumatoid arthritis: A systematic review and meta-analysis.

Rheumatoid arthritis (RA) is a chronic autoimmune disease caused by established chronic inflammation. Neopterin levels have extensively been considered as a marker of immune activation during inflammation. In this study, we performed a systematic evaluation and meta-analysis to elucidate the overall relationship between neopterin concentration and RA disease activity. Following the Preferred Reporting Items for Systematic Reviews and Meta-Analysis guidelines, a systematic review was conducted using PubMed, Google Scholar, Web of Science, and Scopus from 2000 to August 2020. The Newcastle-Ottawa scale was used to assess the quality of eligible studies. The effect size (ES) and corresponding 95% confidence intervals (CIs) were calculated to evaluate this association. A total of 15 studies out of 98 met our inclusion criteria. The pooled analysis found that patients with RA had high level of neopterin; however, no statistically significant association was found between neopterin levels with high, intermediate, and low diseases activity score (DAS)-28 (ES =11.18, 95% CI: 6.02 to 16.34, and I2 = 91.8%; and ES = 8.57, 95% CI: 6.41 to 10.37, and I2 = 99.5%; and ES =12.45, 95% CI: -1.68 to 26.58, and I2 = 99.0%, respectively). Our results indicated that the neopterin concentration does not seem to have any substantial impact on the RA disease activity.