Christopher D. Hammerbeck

Matthew F. Mescher

Abstract
               The high-affinity chain of the IL-7 receptor, IL-7Rα (CD127), is expressed by effector CD8 T cells that have the capacity to become memory cells. IL-7Rα 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-7Rα 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-7Rα have not been fully defined. In vitro experiments demonstrated that Ag alone is sufficient to down-regulate IL-7Rα 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-7Rα expression. Consistent with this, in vivo priming with peptide Ag resulted in IL-7Rα 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-7Rα, but most of these cells failed to survive; those that did survive expressed high IL-7Rα levels. Thus, Ag-dependent signals regulate IL-7Rα 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.</jats:p

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

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