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Abstract
A key role for segmented filamentous bacteria (SFB) has recently been demonstrated in several mouse models of autoimmune diseases, including autoimmune arthritis and multiple sclerosis. The mechanism governing the activation of systemic autoreactive T cell responses by such commensals in the gut, however, remained elusive. In this addendum, we discuss recent results addressing the local regulation of autoreactive T cell sensitivity by these unique bacteria. We found that the presence of SFB in the gut microbiota was sufficient to promote a local inflammatory microenvironment altering the T cell-intrinsic desensitization process normally occurring in response to chronic self-antigen stimulation. In the absence of this key tolerance checkpoint, sustained chronic T cell proliferation, IFNγ production, and B cell activation eventually led to the development of enhanced pathologies in a Th1-driven T cell-transfer model of autoimmune arthritis.
Disclosure of Potential Conflicts of Interest
No potential conflict of interest was disclosed.
Acknowledgments
The author would like to thank RH Schwartz, DA Gross, and M Lalfer for helpful comments on the manuscript and figures. The original work was supported by the Intramural Research Program of the NIAID at the National Institutes of Health, Bethesda, MD, USA. The author also acknowledges funding support from Agence Nationale de la Recherche (ANR-11-JSV3-0005).