The Journal of Experimental Medicine
VeriKine-HS Human IFN-Beta
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© The Rockefeller University Press, 0022-1007/1997/2/641/ $5.00
The Journal of Experimental Medicine, Volume 185, Number 4, February 17, 1997 641-652

Articles

Requirements for Peptide-induced T Cell Receptor Downregulation on Naive CD8+ T Cells

Zeling Cai{ddagger}, Hidehiro Kishimoto*, Anders Brunmark{ddagger}, Michael R. Jackson{ddagger}, Per A. Peterson{ddagger}, and Jonathan Sprent*

From the * Department of Immunology, IMM4, The Scripps Research Institute, La Jolla, California 92037; and {ddagger} R.W. Johnson Pharmaceutical Research Institute, San Diego, California 92121

The requirements for inducing downregulation of {alpha}/β T cell receptor (TCR) molecules on naive major histocompatibility complex class I–restricted T cells was investigated with 2C TCR transgenic mice and defined peptides as antigen. Confirming previous results, activation of 2C T cells in response to specific peptides required CD8 expression on the responder cells and was heavily dependent upon costimulation provided by either B7-1 or ICAM-1 on antigen-presenting cells (APC). These stringent requirements did not apply to TCR downregulation. Thus, TCR downregulation seemed to depend solely on TCR/peptide/interaction and did not require either CD8 or B7-1 expression; ICAM-1 potentiated TCR downregulation, but only with limiting doses of peptides. TCR downregulation was most prominent with high affinity peptides and appeared to be neither obligatory nor sufficient for T cell activation. In marked contrast to T cell activation, TCR downregulation was resistant to various metabolic inhibitors. The biological significance of TCR downregulation is unclear, but could be a device for protecting T cells against excessive signaling.

Address correspondence to Jonathan Sprent, Department of Immunology, IMM4, The Scripps Research Institute, 10550 North Torrey Pines Rd., La Jolla, CA 92037.

1Abbreviations used in this paper: CCD, cytochalasin D; i, internal; s, surface.


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