Journal
NATURE IMMUNOLOGY
Volume 14, Issue 3, Pages 271-280Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/ni.2518
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Funding
- Ellison Medical Foundation
- Irma T. Hirschl Trust
- Crohn's & Colitis Foundation of America
- US National Institutes of Health [R01 DK093674-01]
- Leona M. and Harry B. Helmsley Charitable Trust
- Fundacao de Amparo a Pesquisa do Estado de Sao Paulo
- Conselho Nacional de Desenvolvimento Cientifico e Tecnologico
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The gut mucosa hosts large numbers of activated lymphocytes that are exposed to stimuli from the diet, microbiota and pathogens. Although CD4(+) T cells are crucial for defense, intestinal homeostasis precludes exaggerated responses to luminal contents, whether they are harmful or not. We investigated mechanisms used by CD4(+) T cells to avoid excessive activation in the intestine. Using genetic tools to label and interfere with T cell development transcription factors, we found that CD4(+) T cells acquired the CD8-lineage transcription factor Runx3 and lost the CD4-lineage transcription factor ThPOK and their differentiation into the T(H)17 subset of helper T cells and colitogenic potential, in a manner dependent on transforming growth factor-beta (TGF-beta) and retinoic acid. Our results demonstrate considerable plasticity in the CD4(+) T cell lineage that allows chronic exposure to luminal antigens without pathological inflammation.
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