Immunoregulatory functions of paf-acether. VI. Inhibition of T cell activation via CD3 and potentiation of T cell activation via CD2

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Abstract
In the present report we further explored the role of paf-acether (paf), a phospholipid cytokine, in the modulation of T cell activation Induced via the CD2 and the CD3 pathways. Evidence was obtained that paf inhibited T cell proliferation Induced by Immobilized CD3 mAb (OKT3I), but potentiated that Induced by a combination with the CD2 mAb, anti-(T11.1 + D66). Both effects were dose-dependent between 2 and 10 μM paf, and specific in that lysoPC, a phospholipid closely related to paf, had no effect. The inhibition became apparent after 48 h and was maintained up to 144 h of culture, whereas the enhancement was observed only by 96 h of culture. Interestingly, paf was able to inhibit OKT3I mAb response when added to cultures as late as 24–48 h after the initiation of a 96 h Incubation. By contrast, paf enhanced the prollferatlve response only when added concomitantly with antl-(T11.1 + D66) mAb, suggesting that it modulates an early event of T cell activation, paf, which enhanced T cell proliferation induced via the CD2 pathway, also led to a substantial up-regulatlon of IL-2 secretion and CD25 expression. Moreover, paf markedly augmented IL-4 secretion upon CD2 mAb stimulation. Finally, when T cells were triggered via the CD3 molecule, paf Inhibited the prollferative response but also down-modulated CD25 expression without impairing IL-2 secretion. When considered together, these data demonstrate that paf, a phospholipid cytokine released during Inflammatory reactions, play a differential regulatory role in T cell activation induced via the CD3 and CD2 (T11.1 + D66) pathways.

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