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* Division of Rheumatology, Department of Pediatrics, Medical College of Wisconsin, Milwaukee, WI 53226; and
Division of Immunology, Allergy and Rheumatology, Department of Pediatrics, David Geffen School of Medicine at the University of California at Los Angeles, Los Angeles, CA 90095
The population dynamics that enable a small number of regulatory T (TR) cells to control the immune responses to foreign Ags by the much larger conventional T cell subset were investigated. During the primary immune response, the expansion and contraction of conventional and TR cells occurred in synchrony. Importantly, the relative accumulation of TR cells at peak response significantly exceeded that of conventional T cells, reflecting extensive cell division within the TR cell pool. Transfer of a polyclonal TR cell population before immunization antagonized both polyclonal and TCR transgenic responses, whereas blocking TR cell function enhanced those responses. These results define an inverse quantitative relationship between TR and conventional T cells that controls the magnitude of the primary immune response. The high frequency of dividing TR cells suggests degenerate TCR specificity enabling activation by a broad spectrum of Ags.
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1 This work was supported by National Institutes of Health Grants 2R01AI065617 (to T.A.C.) and R01 AI47154 (to C.B.W.), and by the Nickolett Family Foundation and the D.B. and Marjorie Reinhart Family Foundation (to C.B.W.).
2 Address correspondence and reprint requests to Dr. Talal A. Chatila, Division of Immunology, Allergy and Rheumatology, Department of Pediatrics, The David Geffen School of Medicine at the University of California at Los Angeles, MDCC 12-430, 10833 Le Conte Avenue, Los Angeles, CA 90095; E-mail address: tchatila{at}mednet.ucla.edu or Dr. Calvin B. Williams, Division of Rheumatology, Department of Pediatrics, Medical College of Wisconsin, 8701 Watertown Plank Road, Milwaukee, WI 53226; E-mail address: cwilliam{at}mcw.edu
3 Abbreviations used in this paper: TR, regulatory T; EGFP, enhanced GFP; IRES, internal ribosomal entry sequence; WT, wild type; R, responder cell; S, suppressor cell.
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