Furue M, Kawakami Y, Kawakami T, Katz S I
Dermatology Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892.
Transplantation. 1990 Mar;49(3):560-4. doi: 10.1097/00007890-199003000-00017.
We examined the inhibitory capacity of dexamethasone (DEX) and cyclosporine (CsA) on T cell activation using various accessory cell (AC)-dependent and AC-independent stimuli. We found that CsA strongly inhibited T cell activation in each of the assays used: allogeneic T cell stimulation, phorbol myristate acetate plus concanavalin A, PMA plus anti-CD3 monoclonal antibody (2C11), or PMA plus ionomycin (IONO) T cell activation. DEX was a potent inhibitor of allogeneic stimulation and of the PMA+Con A- or PMA + 2C11-induced T cell stimulation. PMA + IONO stimulation, however, was not affected by DEX. When inhibition occurred, both drugs suppressed [3H]TdR incorporation, IL-2 production, and IL-2 mRNA accumulation, indicating that the sites of interference of these drugs in the T cell activation pathway are located proximal to IL-2 mRNA accumulation. However, the difference in the effects of DEX and CsA in PMA + IONO stimulation suggests that DEX and CsA differentially affect T cell activation.
我们使用各种辅助细胞（AC）依赖性和AC非依赖性刺激，研究了地塞米松（DEX）和环孢素（CsA）对T细胞活化的抑制能力。我们发现，在所用的每种检测方法中，CsA都强烈抑制T细胞活化：同种异体T细胞刺激、佛波醇肉豆蔻酸酯乙酸酯加刀豆蛋白A、PMA加抗CD3单克隆抗体（2C11）或PMA加离子霉素（IONO）诱导的T细胞活化。DEX是同种异体刺激以及PMA+Con A或PMA + 2C11诱导的T细胞刺激的有效抑制剂。然而，PMA + IONO刺激不受DEX影响。当发生抑制时，两种药物均抑制[3H]TdR掺入、IL-2产生和IL-2 mRNA积累，表明这些药物在T细胞活化途径中的干扰位点位于IL-2 mRNA积累的近端。然而，DEX和CsA在PMA + IONO刺激中的作用差异表明，DEX和CsA对T细胞活化的影响不同。
