PHOSPHOANTIGEN ACTIVATION INDUCES SURFACE TRANSLOCATION OF INTRACELLULAR CD94 NKG2A CLASS-I RECEPTOR ON CD94(-) PERIPHERAL V-GAMMA-9 V-DELTA-2 T-CELLS BUT NOT ON CD94(-) THYMIC OR MATURE GAMMA-DELTA T-CELL CLONES/

Most adult peripheral blood gamma delta T cells express V gamma 9/V de lta 2-encoded TCR that recognize a restricted set of nonpeptidic phosp horylated compounds, referred to as phosphoantigens. They also express various MHC class I-specific inhibitory receptors (IR), in particular CD94/NKG2-A heterodimers, which participate in the fine tuning of the ir TCR-mediated activation threshold. Most mature V gamma 9/V delta 2 T cells express surface CD94 receptors, unlike cord blood or thymus-de rived V gamma 9/V delta 2 clones, thus suggesting a role for the micro environment in IR expression. In the present study we show that most C D94(-) V gamma 9V delta 2 PBL ex vivo express an intracellular pool of CD94/NKG2-A receptors that is translocated to the cell surface upon a ctivation by phosphoantigens or IL-2. In stark contrast, intracellular CD94/NKG2-A complexes are undetectable in CD94(-) thymus or PBL-deriv ed mature V delta 2 T cell clones, and no surface induction is observe d following phosphoantigen activation of T cell clones. Altogether the se results provide new insights into the regulation of CD94/NKG2-A exp ression on T lymphocytes and suggest the existence of distinct mechani sms controlling in vivo and in vitro induction of IR on these cells.