艾滋病病毒入侵后，人体免疫细胞的功能会受到削弱，科学家最近发现了其中的机理。这一发现将有助于人们找到治疗艾滋病的新方法。
据最新一期英国《自然·医学》杂志报道，美国波士顿马萨诸塞综合医院的一个研究小组对南非71名未接受过治疗的艾滋病患者的“CD8”免疫细胞进行检测后发现，病人体内艾滋病病毒越多，“CD8”表面上一种名为“PD-1”的受体越多。但当研究人员给病人服用抗逆转录病毒药物以大量抑制病人血液中的病毒数量后，病人“CD8”细胞表面的“PD-1”受体数量也随之减少。
研究人员解释说，艾滋病病毒增加，会使免疫细胞“CD8”开始大量产生“PD-1”受体。随着这种受体在免疫细胞表面堆积，免疫细胞功能变弱，只能产生很少的化学物质来杀死病毒。
加拿大蒙特利尔中心医院的一个研究小组对19名北美病人的研究也得出了同样的结果。
据报道，两个研究小组都成功利用“PD-1”受体的抗体，以帮助免疫细胞“CD8”恢复正常功能。在实验过程中，经过处理的免疫细胞“CD8”恢复了正常活力，生产出了可以攻击艾滋病病毒的γ干扰素等化学物质。研究人员目前在实验鼠身上已经证明了这一方法的有效性，希望下一步能尽快进行人体实验。
部分英文原文：
Upregulation of PD-1 expression on HIV-specific CD8+ T cells leads to reversible immune dysfunction
The engagement of programmed death 1 (PD-1) to its ligands, PD-L1 and PD-L2, inhibits proliferation and cytokine production mediated by antibodies to CD3 . Blocking the PD-1–PD-L1 pathway in mice chronically infected with lymphocytic choriomeningitis virus restores the capacity of exhausted CD8+ T cells to undergo proliferation, cytokine production and cytotoxic activity and, consequently, results in reduced viral load8. During chronic HIV infection, HIV-specific CD8+ T cells are functionally impaired, showing a reduced capacity to produce cytokines and effector molecules as well as an impaired capacity to proliferate. Here, we found that PD-1 was upregulated on HIV-specific CD8+ T cells; PD-1 expression levels were significantly correlated both with viral load and with the reduced capacity for cytokine production and proliferation of HIV-specific CD8+ T cells. Notably, cytomegalovirus (CMV)-specific CD8+ T cells from the same donors did not upregulate PD-1 and maintained the production of high levels of cytokines. Blocking PD-1 engagement to its ligand (PD-L1) enhanced the capacity of HIV-specific CD8+ T cells to survive and proliferate and led to an increased production of cytokines and cytotoxic molecules in response to cognate antigen. The accumulation of HIV-specific dysfunctional CD8+ T cells in the infected host could prevent the renewal of a functionally competent HIV-specific CD8+ repertoire.
