The Journal of Experimental Medicine
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© The Rockefeller University Press, 0022-1007/1997/11/1769/ $5.00
The Journal of Experimental Medicine, Volume 186, Number 10, November 17, 1997 1769-1774

Brief Definitive Reports

Major Histocompatibility Complex Class I Molecules Modulate Activation Threshold and Early Signaling of T Cell Antigen Receptor–{gamma}/{delta} Stimulated by Nonpeptidic Ligands

Ilaria Carena*, Abdijapar Shamshiev*, Alena Donda*, Marco Colonna{ddagger}, and Gennaro De Libero*

From * Experimental Immunology, Department of Research, University Hospital, CH-4031 Basel, Switzerland; and {ddagger} Basel Institute for Immunology, CH-4005 Basel, Switzerland

Killer cell inhibitory receptors and CD94-NKG2-A/B heterodimers are major histocompatibility complex class I–specific inhibitory receptors expressed by natural killer cells, T cell antigen receptor (TCR)-{gamma}/{delta} cells, and a subset of TCR-{alpha}/β cells. We studied the functional interaction between TCR-{gamma}/{delta} and CD94, this inhibitory receptor being expressed on the majority of {gamma}/{delta} T cells. When engaged by human histocompatibility leukocyte antigen class I molecules, CD94 downmodulates activation of human TCR-{gamma}/{delta} by phosphorylated ligands. CD94-mediated inhibition is more effective at low than at high doses of TCR ligand, which may focus T cell responses towards antigen-presenting cells presenting high amounts of antigen. CD94 engagement has major effects on TCR signaling cascade. It facilitates recruitment of SHP-1 phosphatase to TCR–CD3 complex and affects phosphorylation of Lck and ZAP-70 kinase, but not of CD3 {zeta} chain upon TCR triggering. These events may cause abortion of proximal TCR-mediated signaling and set a higher TCR activation threshold.

Address correspondence to Dr. Gennaro De Libero, Experimental Immunology, Department of Research, University Hospital, Hebelstrasse 20, CH-4031 Basel, Switzerland. Phone: 41-61-265-2327; FAX: 41-61-265-2350.

The Basel Institute for Immunology was founded and is supported by F. Hoffmann-La Roche Ltd. This work was supported by Swiss National Fund grant 31-045518.95 to G. De Libero.


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