Journal
NATURE COMMUNICATIONS
Volume 9, Issue -, Pages -Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/s41467-017-02406-2
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Funding
- Research Project on Rare and Intractable Diseases, Health, Labour and Welfare Sciences Research
- Ministry of Health, Labour and Welfare of Japan [H26-itaku(nan)-ippan-019]
- Practical Research Project for Rare/Intractable Diseases from Japan Agency for Medical Research and Development, AMED [15ek0109097h0001, 16ek0109097h0002]
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Multiple sclerosis (MS) is a T cell-mediated autoimmune disease of the central nervous system. Foxp3(+) regulatory T (Treg) cells are reduced in frequency and dysfunctional in patients with MS, but the underlying mechanisms of this deficiency are unclear. Here, we show that induction of human IFN-gamma-IL-17A(-)Foxp3(+)CD4(+) T cells is inhibited in the presence of circulating exosomes from patients with MS. The exosomal miRNA profile of patients with MS differs from that of healthy controls, and let-7i, which is markedly increased in patients with MS, suppresses induction of Treg cells by targeting insulin like growth factor 1 receptor (IGF1R) and transforming growth factor beta receptor 1 (TGFBR1). Consistently, the expression of IGF1R and TGFBR1 on circulating naive CD4(+)T cells is reduced in patients with MS. Thus, our study shows that exosomal let-7i regulates MS pathogenesis by blocking the IGF1R/TGFBR1 pathway.
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