Myeloid-derived suppressor cells (MDSCs) are a heterogeneous group of the immature myeloid cells that are derived from the myeloid progenitors with immunosuppressive functions. MDSCs are accumulated in the inflammatory sites during some autoimmune disorders, such as rheumatoid arthritis (RA) and can be an important factor in the pathogenesis of these diseases. Some research has shown the anti-inflammatory role of MDSCs during the RA progression and supports the hypothesis that MDSCs can be a potential treatment option for autoimmunity with their immunosuppressive activity. In contrast, some papers have reported the opposite effects of MDSCs, and support the hypothesis that MDSCs have a pro-inflammatory role in autoimmune disease. MDSCs functions in RA have not been fully understood, and some controversies, as well as many unanswered questions, remain. Although the two well-known subgroups of MDSCs, M-MDSC, and PMN-MDSC, seem to have different suppressive functions and regulate the immune system responses in a different manner; some studies have shown these cells are converted to each other and even to other cells under different pathological conditions. This review summarises some of the latest papers with respect to the MDSCs functions and discusses the relationship between MDSCs and inflammation in the context of rheumatoid arthritis. Graphical Abstract

Diabetic neuropathy (DN) is a prevalent complication of diabetes mellitus characterized by pain and inflammation. Long non-coding RNAs (lncRNAs) have been associated with DN. This study aimed to investigate transcript levels of Metastasis-associated lung adenocarcinoma transcript 1 (MALAT1), microRNA (miR)-1-3p, and C-X-C motif chemokine receptor 4 (CXCR4) in the DN patients and type 2 diabetes mellitus (T2DM) cases without neuropathy. Here, 20 cases with DN and 20 T2DM subjects without neuropathy (as the control group) were included. Total RNA was extracted from peripheral blood mononuclear cells (PBMCs) of all participants. The expression levels of targets were evaluated by Real-time-PCR. Results showed that MALAT1 (Fold change = 2.47, P = 0.03) and CXCR4 (Fold change = 1.65, P = 0.023) were significantly upregulated, while miR-1-3p was downregulated (Fold change = 0.9, P = 0.028) in whole blood samples from DN patients compared to the control group. A significant correlation was found between transcript levels of MALAT1 and CXCR4 (rho = 0.84; P < 0.0001). This study suggests a possible involvement of the MALAT1/miR-1-3p/CXCR4 axis in the pathogenesis of DN.

Allergic rhinitis (AR) is a T helper type 2 (Th2)-mediated upper airways disease in which genetics factors including cytokine genes play a prominent role. Interleukin-33 (IL-33) is a major cytokine...