Dr Evelyn Tsantikos, Research Officer in A/Prof Margaret Hibbs' group |
Recent studies have shown that alterations in gut microbiota (dysbiosis) can lead to many autoimmune diseases, including diseases with clear association to the gut, notably inflammatory bowel disease. However, the cellular and molecular mechanisms by which microbiota in the gut influence systemic autoimmune diseases such as rheumatoid arthritis (RA) remain largely unknown.
The authors demonstrate that a type of commensal gut bacteria, segmented filamentous bacteria (SFB), triggers autoimmune arthritis by inducing differentiation and migration of gut T follicular helper cells to systemic lymphoid sites, leading to increased autoantibody production and exacerbation of arthritis. SFB increased the Tfh cell population not only in Peyer’s patches (PP), a gut-associated lymphoid tissue, but also in systemic sites such as the spleen and foot-draining popliteal lymph nodes. SFB induced PP Tfh cell differentiation by inhibiting the IL-2 signaling pathway in PPs and identified DCs as the critical cell type required for SFB-mediated Tfh cell induction.
Their work proposes a mechanism by which gut microbiota contribute to gut-distal autoimmune arthritis by triggering the induction and migration of gut Tfh cells into systemic sites.
Don’t miss it: Thursday, 16 June 2016 at 12.00pm in Seminar Room One, level 5 Alfred Centre.
Snacks will be provided
Enquiries to Menno van Zelm, Email menno.vanzelm@monash.edu
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