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Immunotherapy with iTreg and nTreg Cells in a Murine Model of Inflammatory Bowel Disease

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Part of the book series: Methods in Molecular Biology ((MIMB,volume 1422))

Abstract

Regulatory T (Treg) cells that express the transcription factor Foxp3 are essential for maintaining tolerance at mucosal interfaces, where they act by controlling inflammation and promoting epithelial cell homeostasis. There are two major regulatory T-cell subsets, “natural” CD4+ Treg (nTreg) cells that develop in the thymus and “induced” Treg (iTreg) cells that develop from conventional CD4+ T (Tconv) cells in the periphery. Dysregulated Treg cell responses are associated with autoimmune diseases, including inflammatory bowel disease (IBD) and arthritis. Adoptive transfer of Treg cells can modulate innate and adaptive immune responses and cure disease in animal models, which has generated considerable interest in using Treg cells to treat human autoimmune disease, prevent rejection of transplanted organs, and to control graft-versus-host disease following hematopoietic stem cell transplantation. Herein, we describe our modifications of a treatment model of T-cell transfer colitis designed to allow mechanistic investigation of the two major Treg cell subsets and to compare their specific roles in mucosal tolerance.

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Acknowledgement

This work was supported by Senior Research Award #296598 from the Crohn’s and Colitis Foundation of America (to C.B.W.), NIH R01 AI073731 and R01 AI085090 (to C.B.W. and T.A.C.), the D.B. and Marjorie Reinhart Family Foundation (to C.B.W.), and the Children’s Hospital of Wisconsin (to C.B.W.).

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Correspondence to Calvin B. Williams .

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Haribhai, D., Chatila, T.A., Williams, C.B. (2016). Immunotherapy with iTreg and nTreg Cells in a Murine Model of Inflammatory Bowel Disease. In: Ivanov, A. (eds) Gastrointestinal Physiology and Diseases. Methods in Molecular Biology, vol 1422. Humana Press, New York, NY. https://doi.org/10.1007/978-1-4939-3603-8_19

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  • DOI: https://doi.org/10.1007/978-1-4939-3603-8_19

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  • Publisher Name: Humana Press, New York, NY

  • Print ISBN: 978-1-4939-3601-4

  • Online ISBN: 978-1-4939-3603-8

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