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Original Article

^a Mucosal Immunity Section, Laboratory of Clinical Investigation, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892
National Institutes of Health, Building 10, Rm. 11N238, 10 Center Dr., Bethesda, MD 20892.301-402-2240301-496-6810

wstrober{at}niaid.nih.gov

CD4⁺CD25⁺ T cells have been identified as a population of immunoregulatory T cells, which mediate suppression of CD4⁺CD25^– T cells by cell–cell contact and not secretion of suppressor cytokines. In this study, we demonstrated that CD4⁺CD25⁺ T cells do produce high levels of transforming growth factor (TGF)-β1 and interleukin (IL)-10 compared with CD4⁺CD25^– T cells when stimulated by plate-bound anti-CD3 and soluble anti-CD28 and/or IL-2, and secretion of TGF-β1 (but not other cytokines), is further enhanced by costimulation via cytotoxic T lymphocyte–associated antigen (CTLA)-4. As in prior studies, we found that CD4⁺CD25⁺ T cells suppress proliferation of CD4⁺CD25^– T cells; however, we observed here that such suppression is abolished by the presence of anti–TGF-β. In addition, we found that CD4⁺CD25⁺ T cells suppress B cell immunoglobulin production and that anti–TGF-β again abolishes such suppression. Finally, we found that stimulated CD4⁺CD25⁺ T cells but not CD4⁺CD25^– T cells express high and persistent levels of TGF-β1 on the cell surface. This, plus the fact that we could find no evidence that a soluble factor mediates suppression, strongly suggests that CD4⁺CD25⁺ T cells exert immunosuppression by a cell–cell interaction involving cell surface TGF-β1.

Key Words: T lymphocytes, suppressor-effector • CD4-positive T lymphocytes • receptors, interleukin 2 • transforming growth factors • autoimmune diseases

© 2001 The Rockefeller University Press

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This article has been cited by other articles:

• Lee, J. H., Wang, C., Kim, C. H. (2009). FoxP3+ Regulatory T Cells Restrain Splenic Extramedullary Myelopoiesis via Suppression of Hemopoietic Cytokine-Producing T Cells. J. Immunol. 183: 6377-6386 [Abstract] [Full Text]  

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