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Rapid expansion of Treg cells protects from collateral colitis following a viral trigger

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Beatriz Gomez del Amo

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Beatriz Gomez del Amo

Regulatory T (Treg) cells are important for the induction and maintenance of peripheral tolerance; therefore, they are key in preventing excessive immune responses and autoimmunity and are responsible for maintaining homeostasis. Treg cells contribute to the complex pathogenesis of inflammatory bowel disease (IBD), including Crohn’s disease and ulcerative colitis during onset or development. Many animal models of IBD have been used to investigate factors such as pathogenic cytokines, pathogenic bacteria, and T-cell functions, including those of Treg cells (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4734996/).

An article published in Nature in March 2020 by Schorer and colleagues (https://www.nature.com/articles/s41467-020-15309-6) uncovered an essential role for induced Treg (iTreg) cells expressing specific Vβ chains in preventing autoimmunity upon viral triggers. LCMV infection induces a type I interferon-dependent loss of Treg cells, which is rapidly compensated for by the conversion of high-affinity Vβ5+ conventional T cells into iTreg cells. While these Vβ5+ iTreg cells do not play a role in limiting the anti-viral immune response, they are essential for suppression of colitogenic CD8+ effector T cells at the gut barrier site. In humans, this role is fulfilled by Vβ2+ Treg cells, which are specifically expanded in IBD patients with inactive disease. Their results support the concept that the Treg compartment as a whole is able to adapt to inflammatory insults that may compromise peripheral tolerance.

Synexa Life Sciences offers a wide range of panels to assess T cell functional profiles to support clients in pre-clinical and clinical research.  We offer a comprehensive array of flow cytometry, soluble biomarker and genetic assays to measure a multitude of relevant markers in a clinical setting.

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