J. Exp. Med., Volume 186, Number 10, November 17, 1997 1769-1774

BRIEF DEFINITIVE REPORT:
Major Histocompatibility Complex Class I Molecules Modulate Activation Threshold and Early Signaling of T Cell Antigen Receptor-/ Stimulated by Nonpeptidic Ligands

By Ilaria Carena,^* Abdijapar Shamshiev,^* Alena Donda,^* Marco Colonna, and Gennaro De Libero^*

From ^* Experimental Immunology, Department of Research, University Hospital, CH-4031 Basel, Switzerland; and  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)-/ cells, and a subset of TCR-/ cells. We studied the functional interaction between TCR-/ and CD94, this inhibitory receptor being expressed on the majority of / T cells. When engaged by human histocompatibility leukocyte antigen class I molecules, CD94 downmodulates activation of human TCR-/ 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  chain upon TCR triggering. These events may cause abortion of proximal TCR-mediated signaling and set a higher TCR activation threshold.

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