Of Mice and Men: Defining the Role of Interleukin 17 in Rheumatoid Arthritis

Ruderman, Eric

doi:10.3899/jrheum.150554

Cited by 1 publication

(1 citation statement)

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“…These differences certainly reflect the different arthritogenic mechanisms in different models. They are also mirrored in several clinical trials testing anti-IL-17 and anti-IL-17R antibodies in rheumatoid arthritis patients that demonstrated only weak to moderate efficacy (32–35). …”

Section: Discussionmentioning

confidence: 79%

Gut Microbiota Regulates K/BxN Autoimmune Arthritis through Follicular Helper T but Not Th17 Cells

Block

Zheng

Dent

et al. 2016

The Journal of Immunology

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The bacterial community that colonizes mucosal surfaces helps shape the development and function of the immune system. The K/BxN autoimmune arthritis model is dependent on the microbiota, and particularly on segmented filamentous bacteria (SFB), for the autoimmune phenotype. The mechanisms of how the gut microbiota affects arthritis development are not well understood. Here we investigate the contribution of two T cell subsets, Th17 and Tfh, to arthritis and how microbiota modulates their differentiation. Using genetic approaches, we demonstrate that IL-17 is dispensable for arthritis. Antibiotic treatment inhibits disease in IL-17 deficient animals suggesting that the gut microbiota regulates arthritis independent of Th17 cells. In contrast, conditional deletion of Bcl6 in T cells blocks Tfh cell differentiation and arthritis development. Furthermore, Tfh cell differentiation is defective in antibiotic-treated mice. Taken together, we conclude that gut microbiota regulates arthritis through Tfh but not Th17 cells. These findings have implications in our understanding of how environmental factors contribute to the development of autoimmune diseases.

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Section: Discussionmentioning

confidence: 79%