NIH VideoCast - Triggering murine arthritis by a single commensal microbe

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Triggering murine arthritis by a single commensal microbe

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Air date:	Wednesday, May 26, 2010, 4:15:00 PM Time displayed is Eastern Time, Washington DC Local
Views:	Total views: 191 * This only includes stats from October 2011 and forward.
Category:	Immunology
Runtime:	01:00:05
Closed captioning:	Check box to display CC outside of the video Note: You can drag the captioning window around and resize it
Description:	Commensal microbes can have a substantial impact on autoimmune disorders, but the underlying molecular and cellular mechanisms remain largely unexplored. We report that autoimmune arthritis was strongly attenuated in the K/BxN mouse model under germ-free (GF) conditions, accompanied by reductions in serum-autoantibody titers, splenic autoantibody-secreting cells, germinal centers and the splenic T helper (Th)17 cell population. Neutralization of interleukin-17 prevented arthritis development in specific-pathogen-free K/BxN mice due to a direct effect of this cytokine on B cells to inhibit germinal center formation. The systemic immune-system deficiencies of the GF animals reflected a loss of Th17 cells from the small-intestinal lamina-propria in the absence of gut microbiota. Introduction of a single gut-residing species, segmented filamentous bacteria, into GF K/BxN animals reinstated the lamina-propria Th17 compartment, and arthritis rapidly ensued. Thus, a single commensal microbe, via its ability to promote a specific Th-cell subset, can drive an autoimmune disease. The Immunology Interest Group

NLM Title:	Triggering murine arthritis by a single commensal microbe / Diane Mathis ; the Immunology Interest Group.
Author:	Mathis, Diane. National Institutes of Health (U.S.). Immunology Interest Group.
Publisher:
Abstract:	(CIT): Commensal microbes can have a substantial impact on autoimmune disorders, but the underlying molecular and cellular mechanisms remain largely unexplored. We report that autoimmune arthritis was strongly attenuated in the K/BxN mouse model under germ-free (GF) conditions, accompanied by reductions in serum-autoantibody titers, splenic autoantibody-secreting cells, germinal centers and the splenic T helper (Th)17 cell population. Neutralization of interleukin-17 prevented arthritis development in specific-pathogen-free K/BxN mice due to a direct effect of this cytokine on B cells to inhibit germinal center formation. The systemic immune-system deficiencies of the GF animals reflected a loss of Th17 cells from the small-intestinal lamina-propria in the absence of gut microbiota. Introduction of a single gut-residing species, segmented filamentous bacteria, into GF K/BxN animals reinstated the lamina-propria Th17 compartment, and arthritis rapidly ensued. Thus, a single commensal microbe, via its ability to promote a specific Th-cell subset, can drive an autoimmune disease.
Subjects:	Arthritis, Experimental--immunology Arthritis, Experimental--microbiology Mice
Publication Types:	Lecture Webcast
NLM Classification:	WE 344
NLM ID:	101535253
CIT Live ID:	8689
Permanent link:	https://videocast.nih.gov/watch=8689

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