Quinnan G V, Siegel J P, Epstein J S, Manischewitz J F, Barnes S, Wells M A
Ann Intern Med. 1985 Nov;103(5):710-4. doi: 10.7326/0003-4819-103-5-710.
Cell-mediated immune responses to cytomegalovirus infections were studied to define mechanisms for deficient effector T-cell responses in patients with the acquired immunodeficiency syndrome (AIDS). Progressive cytomegalovirus infection is common in such patients and is accompanied by a failure to develop HLA-restricted cytotoxic T-cell responses. The mechanism for the cytotoxic T-cell deficiency is presumably the basis for susceptibility to opportunistic infections. Precursors to these effector cells circulate in the peripheral blood of patients, but maturation of these cells into cytotoxic T cells is arrested during an interleukin-2-dependent phase. Production of interleukin-2 by lymphocytes from patients with AIDS is deficient because sera from these patients contain an inhibitor of interleukin-2 production. Excess suppressor cell activity does not appear to account for this deficient production. Studies of the source of the serum inhibitor should provide insights into the pathogenesis of AIDS and possible leads for effective treatment.
为了确定获得性免疫缺陷综合征（AIDS）患者效应T细胞反应缺陷的机制，对巨细胞病毒感染的细胞介导免疫反应进行了研究。进行性巨细胞病毒感染在这类患者中很常见，并伴有无法产生HLA限制性细胞毒性T细胞反应。细胞毒性T细胞缺陷的机制可能是易患机会性感染的基础。这些效应细胞的前体细胞在患者外周血中循环，但这些细胞在白细胞介素-2依赖阶段成熟为细胞毒性T细胞的过程被阻断。AIDS患者淋巴细胞产生白细胞介素-2不足，因为这些患者的血清含有白细胞介素-2产生的抑制剂。过量的抑制细胞活性似乎不能解释这种产生不足的情况。对血清抑制剂来源的研究应该能为AIDS的发病机制提供见解，并为有效治疗提供可能的线索。
