Gut-Residing Segmented Filamentous Bacteria Drive Autoimmune Arthritis via T Helper 17 cells (Immunity, 2010, 32:815-827)

報告日期: 2010/09/21
報告時間: 15:10/16:00
報告學生: 李易丞
講評老師: 林以行

Full Text:

Gut-residing segmented filamentous bacteria drive autoimmune arthritis via T helper 17 cells

Wu HJ, Ivanov II, Darce J, Hattori K, Shima T, Umesaki Y, Littman DR, Benoist C, Mathis D

Immunity. 2010 Jun 25;32(6):815-27.



Date21 Sep, 2010  15:10~16:00

PlaceRoom 602



The gastrointestinal microbiome and immune system are closely tied, each influencing and being influenced by the other. It is believed that commensal microbes can have an impact of autoimmune disorder, but the impact mechanisms remain unexplored. In this study, the authors used specific-pathogen-free and germ-free K/BxN mice, an autoimmune arthritis model, to investigate whether gut-residing microorganisms affect the development of autoimmune arthritis. In the germ-free condition, K/BxN mice have lower serum autoantibody titers, less splenic autoantibody-secreting cells, germinal centers, and the splenic T helper 17 cells than those in specific-pathogen-free K/BxN mice. Introducing gut-residing segmented filamentous bacteria into germ-free K/BxN mice reinstated lamina propria Th17 cell compartment and the production of autoantibodies which induce autoimmune arthritis. These symptoms can be restrained by using antibiotics. Thus the intestine commensal bacteria may play a regulatory role in autoimmune arthritis through stimulating T helper 17 cells accumulation in small intestinal mucosa and the down-stream joint inflammation. Given the fact that antibiotic abuse generates drug resistant microbiomes, using probiotics to increase the beneficial gut microbiomes and decreasing harmful commensal microorganisms (including SFB) may be an effective approach to modulate autoimmune responses.



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