The CD94/NKG2 complex is expressed on T and NK lymphocytes. CD94 molecules covalently associate to activating or inhibitory NKG2 molecules, and their expression finely tunes cell responses. Human γδ T cells express several NKRs. Expression of these receptors is confined to the cytolytic Vδ2 subset, which coexpresses the FcγRIII CD16 and CD45RA and has been defined as Vγ9Vδ2 T(EMRA) cells. We show that the CD94/NKG2C complex, associated with KARAP/DAP12, is fully functional in γδ T cells, as determined by measuring IFN-γ production, T cell proliferation, and cytolytic activity by γδ lymphocytes. In contrast, NKG2A expression was found on all γδ T cell memory subsets, suggesting a crucial role of the inhibitory signal provided by this receptor on γδ T cell responses. Moreover, we found Vγ9Vδ2 T(EMRA), NK, and CD8+ αβ T cells coexpressing NKG2A and NKG2C receptors. Functional experiments showed that the inhibitory signal mediated by the NKG2A receptor prevails when double-positive cells are activated. Finally, NKG2A expression on γδ LDGL correlates with asymptomatic pathology, even in the presence of NKG2C coexpression, whereas in symptomatic patients affected by severe disease, the inhibitory NKG2A receptor is absent, and a variety of activatory NKRs was found. We propose that the silent behavior of γδ cells in LDGL patients is a result of effective inhibitory HLA class I receptors.

T cell immune function in 20 newborn infants was investigated. Previous studies showing increased spontaneous transformation and higher ³H-thymidine incorporation at lower PHA concentration in newborn infants were confirmed. A net increase in the number of active E rosette-forming lymphocytes and a slight decrease in the percentage of total E rosette-forming cells was also found. Our results suggest the presence of a subpopulation of activated T lymphocytes in the peripheral blood of newborns during the first days of life. Possible mechanisms of this activation are discussed.

The lymphocytes blastigenesis to PHA in culture with autologous or normal plasma, the formation of E rosettes and the presence of immunoglob-lins on the lymphocytes surface were evaluated in 51 patients with chronic primary polyarthritis. While the percentage of T and B cells was almost normal (52.1 +/- 2.1% and 18.1 +/- 2.1%, N.V. 55.6 +/- 2.0% and 16.2 +/- 0.8%), the blastigenesis was significantly reduced in cultures with a 25% autologous plasma (5399 +/- 709 cpm compared to 13,182 +/- 920 cpm of the normal standard) and returned towards normal values when it was replaced by the plasma of a normal subject (12,189 +/- 1081 cpm). The rheumatoid plasma was capable of reducing the blastigenesis in 11 normal subjects (7395 +/- 750 cpm). The preincubation for 90' of the lymphocytes of 14 controls in rheumatoid or autologous plasma induced a significant reduction in the formation of spontaneous rosettes (40.8 +/- 1.4 % and 56.2 +/- 1.7%). These results suggest that the reduced function of the T lymphocytes in this disease is due to plasma factors.

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