AI Article Synopsis

  • Multiple sclerosis (MS) is an autoimmune disease affecting the central nervous system, where inflammatory CD4 T cells attack myelin and oligodendrocytes.
  • Regulatory T (Treg) cells, which usually control harmful immune responses, are found to be diminished in MS patients, although the reason is not fully understood.
  • Recent findings suggest that circulating exosomes from MS patients inhibit Treg cell differentiation by transferring specific microRNAs to naive CD4 T cells, potentially linking gut microbiota, immune response, and autoimmune disease development.

Article Abstract

Multiple sclerosis (MS) is an autoimmune disease of the central nervous system, in which myelin and oligodendrocytes are the main targets recognized by inflammatory CD4 T cells reactive to myelin peptides. Regulatory CD4 T (Treg) cells normally keep homeostasis of the immune system by inhibiting detrimental effects of inflammatory T cells. However, Treg cells are reduced in patients with MS for unknown reason. This commentary highlights a novel function of circulating exosomes to inhibit the differentiation of Treg cells in MS. Our recent work has demonstrated that the circulating exosomes, a member of extracellular vesicles, of patients with MS exert this effect by transferring to naive CD4 T cells. The transferred subsequently causes a decreased expression of insulin like growth factor 1 receptor (IGF1R) and transforming growth factor β receptor 1 (TGFBR1), leading to the inhibition of Treg cell differentiation. Thus, extrinsic microRNAs transferred by exosomes might have an active role in triggering autoimmune diseases. We hypothesize that extracellular vesicles including exosomes can be a communication tool between the gut microbiota and the host immune system. Further research in this area will expand the knowledge about the precise mechanism of autoimmune diseases and can lead to a new therapeutic approach.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5881976PMC
http://dx.doi.org/10.1177/1179069518764892DOI Listing

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