The DOI matches its Crossref record; 59 of the 59 references it cites were found in a registry or an index.
Altering the distribution of Foxp3+ regulatory T cells results in tissue-specific inflammatory disease
Open accessAbstract
CD4+Foxp3+ regulatory T cells (T reg) are essential for maintaining self-tolerance, but their functional mechanisms and sites of action in vivo are poorly defined. We examined the homing receptor expression and tissue distribution of T reg cells in the steady state and determined whether altering their distribution by removal of a single chemokine receptor impairs their ability to maintain tissue-specific peripheral tolerance. We found that T reg cells are distributed throughout all nonlymphoid tissues tested, and are particularly prevalent in the skin, where they express a unique CCR4+CD103hi phenotype. T reg cell expression of CCR4 and CD103 is induced by antigen-driven activation within subcutaneous lymph nodes, and accumulation of T reg cells in the skin and lung airways is impaired in the absence of CCR4 expression. Mice with a complete loss of CCR4 in the T reg cell compartment develop lymphocytic infiltration and severe inflammatory disease in the skin and lungs, accompanied by peripheral lymphadenopathy and increased differentiation of skin-tropic CD4+Foxp3+ T cells. Thus, selectively altering T reg cell distribution in vivo leads to the development of tissue-specific inflammatory disease.
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Cites
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Self-citationUlcerative colitis-like disease in mice with a disrupted interleukin-2 gene
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Self-citationRegulatory T Cells Exhibit Distinct Features in Human Breast Cancer
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Metadata
- Authors
- Sather, B. D., Treuting, P., Perdue, N., Miazgowicz, M., Fontenot, J. D., Rudensky, A. Y., & Campbell, D. J.
- Venue
- The Journal of Experimental Medicine
- Publisher
- Rockefeller University Press
- Published
- 2007-06-04
- Volume
- 204
- Issue
- 6
- Pages
- 1335-1347
- ISSN
- 0022-1007 (ISSN-L)
- 1540-9538
- OpenAlex
- W2014540704
- Cited by
- 406
- References
- 59
- FWCI
- 10.86
- Type
- journal article
- Language
- en
- Open access
- bronze
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