Ramírez F, Silva A
Centro de Investigaciones Biológicas, Consejo Superior de Investigaciones Científicas, Madrid, Spain.
Immunology. 1997 Jan;90(1):66-73. doi: 10.1046/j.1365-2567.1997.d01-2134.x.
Glucocorticoids (GC) are known to inhibit mitogen-induced proliferation of T cells. In this study we show two experimental situations where the addition of GC increases lymphocyte proliferation. It has been reported by different authors that rat spleen (SPL) cells proliferate poorly after concanavalin A (Con A) activation. These poor responses have been related to the suppressor activity of macrophages. Similarly, it is known that T-cell proliferation is depressed in the presence of an excess of macrophages in the culture. Here we show that in both experimental situations, the inclusion of dexamethasone (DEX), a synthetic glucocorticoid, in the culture medium enhances the Con A-stimulated proliferation. We provide evidence that this effect is a consequence of the inhibition of nitric oxide (NO) synthesis by the hormone. Furthermore, we also demonstrate that rat SPL cells are inefficient antigen-presenting cells (APC) because of their spontaneous high production of NO. Taken together our results suggest that the effects of GC on T-cell activation may be to promote or inhibit proliferation depending on the level of endogenous NO synthesis. The possible significance of these results is briefly discussed.
已知糖皮质激素（GC）可抑制有丝分裂原诱导的T细胞增殖。在本研究中，我们展示了两种实验情况，即添加GC会增加淋巴细胞增殖。不同作者报道，大鼠脾（SPL）细胞在伴刀豆球蛋白A（Con A）激活后增殖不佳。这些不佳反应与巨噬细胞的抑制活性有关。同样，已知在培养物中存在过量巨噬细胞时T细胞增殖会受到抑制。在此我们表明，在这两种实验情况下，在培养基中加入合成糖皮质激素地塞米松（DEX）可增强Con A刺激的增殖。我们提供的证据表明，这种作用是该激素抑制一氧化氮（NO）合成的结果。此外，我们还证明大鼠SPL细胞由于其自发大量产生NO而不是高效的抗原呈递细胞（APC）。综合我们的结果表明，GC对T细胞活化的影响可能是促进或抑制增殖，这取决于内源性NO合成的水平。简要讨论了这些结果可能的意义。
