NDLI: IL-10 produced by induced regulatory T cells (iTregs) controls colitis and pathogenic ex-iTregs during immunotherapy.

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IL-10 produced by induced regulatory T cells (iTregs) controls colitis and pathogenic ex-iTregs during immunotherapy.

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IL-10 produced by induced regulatory T cells (iTregs) controls colitis and pathogenic ex-iTregs during immunotherapy.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Turner, Amy Broeckel, Ulrich Aggarwal, Praful Ziegelbauer, Jennifer Hessner, Martin J. Williams, Calvin B. Jia, Shuang Yan, Ke Lorier, Rachel Schmitt, Erica G. Chatila, Talal A. Simpson, Pippa Haribhai, Dipica Williams, Jason B. Salzman, Nita H. Georgiev, Peter Charbonnier, Louis-Marie
Description	Country affiliation: United States Author Affiliation: Schmitt EG ( Section of Rheumatology, Department of Pediatrics, Medical College of Wisconsin, Milwaukee, WI 53226, USA.)
Abstract	'Natural' regulatory T cells (nTregs) that express the transcription factor Foxp3 and produce IL-10 are required for systemic immunological tolerance. 'Induced' regulatory T cells (iTregs) are nonredundant and essential for tolerance at mucosal surfaces, yet their mechanisms of suppression and stability are unknown. We investigated the role of iTreg-produced IL-10 and iTreg fate in a treatment model of inflammatory bowel disease. Colitis was induced in Rag1(-/-) mice by the adoptive transfer of naive CD4(+) T cells carrying a nonfunctional Foxp3 allele. At the onset of weight loss, mice were treated with both iTregs and nTregs where one marked subset was selectively IL-10 deficient. Body weight assessment, histological scoring, cytokine analysis, and flow cytometry were used to monitor disease activity. Transcriptional profiling and TCR repertoire analysis were used to track cell fate. When nTregs were present but IL-10 deficient, iTreg-produced IL-10 was necessary and sufficient for the treatment of disease, and vice versa. Invariably, â ¼85% of the transferred iTregs lost Foxp3 expression (ex-iTregs) but retained a portion of the iTreg transcriptome, which failed to limit their pathogenic potential upon retransfer. TCR repertoire analysis revealed no clonal relationships between iTregs and ex-iTregs, either within mice or between mice treated with the same cells. These data identify a dynamic IL-10-dependent functional reciprocity between regulatory T cell subsets that maintains mucosal tolerance. The niche supporting stable iTregs is limited and readily saturated, which promotes a large population of ex-iTregs with pathogenic potential during immunotherapy.
ISSN	00221767
e-ISSN	15506606
DOI	10.4049/jimmunol.1200936
Journal	The Journal of Immunology
Issue Number	12
Volume Number	189
Language	English
Publisher	The American Association of Immunologists
Publisher Date	2012-12-15
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Colitis Immunology Therapy Interleukin-10 Biosynthesis Physiology T-lymphocytes, Regulatory Pathology Animals Animals, Newborn Cell Differentiation Genetics Disease Models, Animal Forkhead Transcription Factors Deficiency Immune Tolerance Inflammatory Bowel Diseases Mice Mice, Inbred Balb C Mice, Knockout Mice, Transgenic Mutagenesis, Insertional Recombinant Fusion Proteins Metabolism Transcriptome Research Support, N.i.h., Extramural Research Support, Non-u.s. Gov't Discipline Immunology
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology

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