Quinacrine inhibits the primary but not secondary proliferative response of human cytotoxic T cells to allogeneic non-T cell antigens.
Quinacrine inhibits the primary but not secondary proliferative response of human cytotoxic T cells to allogeneic non-T cell antigens.
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奎纳克林抑制人细胞毒性 T 细胞对同种异体非 T 细胞抗原的初次增殖反应，但不抑制二次增殖反应。
DOI：
10.4049/jimmunol.132.3.1456
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发表时间：
1984
影响因子：
4.4
通讯作者：
F. Hirata
中科院分区：
文献类型：
--
作者：
S. Namiuchi;S. Kumagai;H. Imura;T. Suginoshita;T. Hattori;F. Hirata
奎纳克林抑制由同种异体非 T 细胞刺激的人外周血 T 细胞产生细胞毒性 T 淋巴细胞，通过 [3H] 胸苷掺入以及针对 51Cr 标记同种异体淋巴细胞的细胞溶解反应来测量。奎纳克林抑制生长因子受体 Tac 抗原的表达进一步支持了这些观察结果。由于其他磷脂酶 A2 抑制剂（例如丁卡因和对溴苯甲酰溴）可以抑制这些反应，因此奎纳克林对细胞毒性 T 淋巴细胞反应的抑制似乎可归因于这些细胞中磷脂酶 A2 的抑制。与这一解释一致，奎纳克林抑制了受同种异体非 T 细胞刺激的细胞毒性 T 细胞中磷脂中花生四烯酸的释放。相比之下，用奎纳克林预处理T细胞并不会抑制其对同种异体非T细胞的相同刺激的二次增殖反应。这些结果综合起来表明，奎纳克林不会抑制细胞毒性 T 细胞对抗原的识别，但会阻断 T 细胞对同种异体抗原的有丝分裂反应。
Quinacrine inhibited the generation of cytotoxic T lymphocytes from human peripheral blood T cells stimulated by allogeneic non-T cells as measured by [3H]thymidine incorporation as well as by cytolytic reactions against 51Cr-labeled allogeneic lymphocytes. These observations were further supported by the finding that quinacrine inhibited the expression of Tac antigen, the receptor for growth factor(s). Because other phospholipase A2 inhibitors such as tetracaine and p-bromophenacyl bromide could inhibit these reactions, the inhibition of cytotoxic T lymphocyte responses by quinacrine appeared to be attributable to the inhibition of phospholipase A2 in these cells. In keeping with this interpretation, arachidonate release from phospholipids in cytotoxic T cells stimulated by allogeneic non-T cells was inhibited by quinacrine. In contrast, the pretreatment of T cells with quinacrine did not result in the inhibition of their secondary proliferative response to the same stimulation with allogeneic non-T cells. These results, taken together, suggest that quinacrine does not inhibit the recognition of antigens by cytotoxic T cells, while it blocks the mitogenic response of T cells to allogeneic antigens.