IL-7 drives Th1 and Th17 cytokine production in patients with primary SS despite an increase in CD4 T cells lacking the IL-7R 

Abstract

IL-7Rα+ cells are highly proliferating cells that respond strongly to IL-7 despite an increased number of IL-7Rα- T cells that express FoxP3 and CD25. The recent finding that IL-7 and IL-7Rα+ T cells were both found to be increased in exocrine glands of pSS patients indicates that IL-7 could contribute to glandular inflammation by activation of IL-7Rα+ responder T cells despite the increased numbers of Tregs.

Decreased microRNA miR-181c expression in peripheral blood mononuclear cells correlates with elevated serum levels of IL-7 and IL-17 in patients with myasthenia gravis

“…Among the potential direct mRNA targets of miR-181c, a number of targets have been identified in murine and in human systems, such as IL-7, IL-1A, IL-1B, TNF-a, IL-25, and IL-16. In this study, we focused on IL-7 as a target gene of miR-181c in view of its role in promoting differentiation and function of multiple effector T cell subsets, especially IFN-c or IL-17-producing T cells [16,21,22]. Experiments with gene-deficient mice indicate that Th17 cells and IL-17 play a crucial role in the pathogenesis of EAMG [23,24].…”

“…The positive correlation between IL-7 and IL-17 may be partly explained by IL-7-induced significant cell proliferation and secretion of IL-17 by PBMCs and CD4(?) T cells [16,34].…”

“…Recent research indicated that IL-7 drives Th17 cytokine production [16], and we also analyzed IL-17 concentration in serum from MG patients. As shown in Fig.…”

Autoantibodies against Muscarinic Acetylcholine Receptor on Exocrine Glands in Sjögren Syndrome

“…In this line, oral and eye sicca symptoms provoking a decrease of the exocrine glandular function are taken as evidence of autoimmunity with the presence of autoantibodies to Ro/SS-A (Ro52, Ro60) or La/SS-B [19,20]. These autoantibodies are non organ specific and their role in the pathogenesis of SS was not been understood yet.…”

“…It is well known that the activation of M 3 mAChR generates the secondary messenger's inositol phosphate (InsP 3 ) and dendritic cells [24]. T cells are balanced toward Th1 and Th17, which release IL-17 [19] and promote the generation of pro-inflammatory cytokines as a main nitric oxide (NO) [25] and as prostaglandins (PG) [11]. This is why PGE 2 and NO together with IL-6 are seen as crucial factors of the maintenance of the inflammatory process and it's becoming chronic [26].…”