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Antigen Controls IL-7R Expression Levels on CD8 T Cells during Full Activation or Tolerance Induction¹

Center for Immunology, Department of Laboratory Medicine and Pathology, University of Minnesota, Minneapolis, MN 55455

The high-affinity chain of the IL-7 receptor, IL-7R (CD127), is expressed by effector CD8 T cells that have the capacity to become memory cells. IL-7R expression is uniformly high on naive CD8 T cells, and the majority of these cells down-regulate expression upon antigenic challenge. At the peak of expansion, the fraction of effectors expressing high IL-7R varies depending on the response examined. The signals that a CD8 T cell receives during a response to Ag that lead to altered expression of IL-7R have not been fully defined. In vitro experiments demonstrated that Ag alone is sufficient to down-regulate IL-7R on all cells and most of the cells rapidly re-express the receptor upon removal from Ag. Expression was not altered by the B7.1 costimulatory ligand or when IL-12 was present to provide the signal needed for development of effector functions, indicating that TCR engagement is sufficient to regulate IL-7R expression. Consistent with this, in vivo priming with peptide Ag resulted in IL-7R expression that inversely correlated with Ag levels, and expression levels were not changed when IL-12 or adjuvant were administered with Ag. A large fraction of the cells present at the peak of expansion had re-expressed IL-7R, but most of these cells failed to survive; those that did survive expressed high IL-7R levels. Thus, Ag-dependent signals regulate IL-7R levels on responding CD8 T cells, and this occurs whether the responding cells become fully activated or are rendered tolerant by administration of peptide Ag alone.

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 R01 AI34824 and P01 AI35296 (to M.F.M).

² Address correspondence and reprint requests to Dr. Matthew F. Mescher, Center for Immunology, Box 334 Mayo, 420 Delaware Street Southeast, Minneapolis, MN 55455. E-mail address: meshc001{at}umn.edu

³ Abbreviations used in this paper: _c, common -chain; LCMV, lymphocyte choriomeningitis virus; LM-OVA, Listeria monocytogenes expressing OVA_257–264; LN, lymph node.