National Eye Institute NEI

Point of Rocks, MD, United States

National Eye Institute NEI

Point of Rocks, MD, United States

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PubMed | National Center for Advancing Translational science, U.S. National Institute on Aging, National Center for Advancing Translational Science, National Cancer Institute NCI and 9 more.
Type: | Journal: Journal of extracellular vesicles | Year: 2015

The Extracellular RNA (exRNA) Communication Consortium, funded as an initiative of the NIH Common Fund, represents a consortium of investigators assembled to address the critical issues in the exRNA research arena. The overarching goal is to generate a multi-component community resource for sharing fundamental scientific discoveries, protocols, and innovative tools and technologies. The key initiatives include (a) generating a reference catalogue of exRNAs present in body fluids of normal healthy individuals that would facilitate disease diagnosis and therapies, (b) defining the fundamental principles of exRNA biogenesis, distribution, uptake, and function, as well as development of molecular tools, technologies, and imaging modalities to enable these studies,


Wang R.-X.,National Eye Institute NEI | Wang R.-X.,Chinese Institute of Basic Medical Sciences | Yu C.-R.,National Eye Institute NEI | Dambuza I.M.,National Eye Institute NEI | And 6 more authors.
Nature Medicine | Year: 2014

Interleukin-10 (IL-10)-producing regulatory B (B reg) cells suppress autoimmune disease, and increased numbers of B reg cells prevent host defense to infection and promote tumor growth and metastasis by converting resting CD4 + T cells to regulatory T (T reg) cells. The mechanisms mediating the induction and development of B reg cells remain unclear. Here we show that IL-35 induces B reg cells and promotes their conversion to a B reg subset that produces IL-35 as well as IL-10. Treatment of mice with IL-35 conferred protection from experimental autoimmune uveitis (EAU), and mice lacking IL-35 (p35 knockout (KO) mice) or defective in IL-35 signaling (IL-12Rβ 22 KO mice) produced less B reg cells endogenously or after treatment with IL-35 and developed severe uveitis. Adoptive transfer of B reg cells induced by recombinant IL-35 suppressed EAU when transferred to mice with established disease, inhibiting pathogenic T helper type 17 (T H 17) and T H 1 cells while promoting T reg cell expansion. In B cells, IL-35 activates STAT1 and STAT3 through the IL-35 receptor comprising the IL-12Rβ 22 and IL-27Rβ± subunits. As IL-35 also induced the conversion of human B cells into B reg cells, these findings suggest that IL-35 may be used to induce autologous B reg and IL-35 + B reg cells and treat autoimmune and inflammatory disease. © 2014 Nature America, Inc. All rights reserved.

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