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CUTTING EDGE |
Center for Immunotherapy of Cancer and Infectious Diseases and Department of Immunology, University of Connecticut Health Center, Farmington, CT 06030
IL-2 is expressed predominantly by activated T cells, and regulates T cell function by activating, via its receptor, the latent transcription factor STAT5. This signaling can occur in either a paracrine (between cells) or an autocrine (same cell) manner, although the kinetics by which these two signaling modes operate during in vivo T cell responses are unknown. In the current study, IL-2 expression and signaling in a clonotypic population of antiviral CD4+ T cells was analyzed by flow cytometry during the initial 24 h of priming. IL-2 expression and STAT5 activation peaked in parallel, but surprisingly, were almost completely mutually exclusive. Thus, only paracrine IL-2 signaling could be observed. As an additional indication of the efficiency of paracrine IL-2 signaling, polyclonal CD4+CD25+Foxp3+ regulatory T cells displayed detectable STAT5 activation under steady-state conditions, which was strongly enhanced by neighboring IL-2-expressing antiviral CD4 cells.
The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
1 This work was supported by National Institutes of Health Grants AI057441 and CA109339 (to A.J.A.).
2 Address correspondence and reprint requests to Dr. Adam J. Adler, Center for Immunotherapy of Cancer and Infectious Diseases, University of Connecticut Health Center, Farmington, CT 06030-1601. E-mail address: aadler{at}up.uchc.edu
3 Abbreviations used in this paper: pSTAT5, phosphorylated STAT5; Treg, CD4+CD25+Foxp3+ regulatory T cell; HA, hemagglutinin; NT, nontransgenic; vacc-HA, recombinant vaccinia expressing HA; PI, PMA + ionomycin.
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