Corlett L, Davies D H
Division of Life Sciences, King's College London, UK.
Immunology. 1995 Mar;84(3):488-94.
The resistance by T lymphocytes to activation by antigen (anergy) is well documented for CD4+ T-helper (Th) cells, although less is known about CD8+ cytotoxic T lymphocytes (CTL). One widely used method of inducing anergy of CD4+Th is presentation of antigen by ECDI (1-ethyl-3-(3-dimethylamino-propyl)carbodiimide)-fixed antigen-presenting cells (APCs). We report here that in murine mixed lymphocyte reactions (MLRs), a marked reduction in detected cytotoxicity (which is mediated predominantly by CD8+ CTL) occurs on day 7 if the bulk cultures are restimulated 2 days previously with ECDI-fixed allogeneic splenocytes. No differences were seen between untreated cultures on days 5 and 7, or on day 7 of cultures to which were added unfixed allogeneic splenocytes, fixed or unfixed syngeneic splenocytes, or 'third-party' allogeneic splenocytes, 2 days previously. The effect is not mediated directly on CD8+ cells, since MLRs depleted of CD4+ cells immediately prior to exposure to fixed allogeneic splenocytes fail to show reduced lysis. On the other hand, reduced lysis did occur if CD4+ cells, purified from the MLRs on day 4, were exposed to ECDI-fixed allogeneic splenocytes and then returned to MLRs previously depleted of CD4+ cells. Moreover the effect is overcome using exogenous interleukin-2 (IL-2). We propose that CD4+ cells, restimulated by a regimen shown previously to induce their anergy, can cause a reduction in CD(8+)-mediated cytotoxicity in MLRs.
T淋巴细胞对抗原激活的抵抗作用(无反应性)在CD4⁺辅助性T细胞(Th细胞)中已有充分记载,尽管对CD8⁺细胞毒性T淋巴细胞(CTL)的了解较少。一种广泛用于诱导CD4⁺Th细胞无反应性的方法是通过用1-乙基-3-(3-二甲基氨基丙基)碳二亚胺(ECDI)固定的抗原呈递细胞(APC)呈递抗原。我们在此报告,在小鼠混合淋巴细胞反应(MLR)中,如果在2天前用ECDI固定的同种异体脾细胞对大量培养物进行再刺激,在第7天检测到的细胞毒性(主要由CD8⁺CTL介导)会显著降低。在第5天和第7天,未处理的培养物之间,或在2天前添加未固定的同种异体脾细胞、固定或未固定的同基因脾细胞或“第三方”同种异体脾细胞的培养物的第7天,均未观察到差异。这种效应不是直接作用于CD8⁺细胞,因为在暴露于固定的同种异体脾细胞之前立即去除CD4⁺细胞的MLR未显示出裂解减少。另一方面,如果将在第4天从MLR中纯化的CD4⁺细胞暴露于ECDI固定的同种异体脾细胞,然后再回到先前已去除CD4⁺细胞的MLR中,则确实会发生裂解减少。此外,使用外源性白细胞介素-2(IL-2)可克服这种效应。我们提出,被先前证明可诱导其无反应性的方案再刺激的CD4⁺细胞,可导致MLR中CD8⁺介导的细胞毒性降低。