期刊
JOURNAL OF EXPERIMENTAL MEDICINE
卷 204, 期 11, 页码 2667-2677出版社
ROCKEFELLER UNIV PRESS
DOI: 10.1084/jem.20062376
关键词
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资金
- NIAID NIH HHS [R01 AI034824, R01 AI34824, R01AI52163, U01AI070380, R01 AI052163, U01 AI070380] Funding Source: Medline
CD8 is critical for T cell recognition of peptide/class I major histocompatability complex ligands, yet is down-regulated during activation of CD8 T cells. We report that loss of CD8 expression early during in vivo responses to vaccinia virus or Listeria monocytogenes (LM) correlates with decreased T cell staining with specific class I/peptide tetramers and reduced CD8 T cell sensitivity for antigen. Loss of CD8 cell surface expression occurs despite sustained mRNA expression, and CD8 levels return to normal levels during differentiation of memory cells, indicating a transient effect. We determined that during response to LM, CD8 down-regulation is regulated by T cell reactivity to type I interferon (IFN-I) because CD8 loss was averted on IFN-I receptor deficient T cells. IFN-I alone was not sufficient to drive CD8 down-regulation, however, as antigen was also required for CD8 loss. These results suggest that CD8 effector T cell differentiation involves a transient down-regulation of antigen sensitivity (CTL detuning), via reduced CD8 expression, a feature that may focus the effector response on target cells expressing high levels of antigen ( e. g., infected cells), while limiting collateral damage to bystander cells.
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