Ebert E C, Stoll D B, Cassens B J, Lipshutz W H, Hauptman S P
Clin Immunol Immunopathol. 1985 Dec;37(3):283-97. doi: 10.1016/0090-1229(85)90099-6.
The Acquired Immunodeficiency Syndrome (AIDS) is a disease found primarily in homosexual men, consisting of opportunistic infections and tumors, and is due to an acquired T-cell defect. In the present report, we studied various T-cell functions which might serve to distinguish homosexuals with a symptom complex including lymphadenopathy from those with AIDS. T lymphocytes from the lymphadenopathy and AIDS patients had markedly depressed proliferative responses in the autologous (auto) and allogeneic (allo) mixed lymphocyte reaction (MLR) compared to healthy homosexuals or heterosexual controls (P less than 0.001). Since proliferation in the MLR depends upon interleukin 2 (IL-2), a T-cell growth factor, we studied the production of and response to IL-2 in various groups of homosexuals and heterosexual controls. IL-2 production was markedly depressed in the lymphadenopathy and AIDS patients, 1.0 and 0.1 U/ml, respectively, compared to the healthy homosexual or heterosexual controls, both 5.0 U/ml (P less than 0.05 and P less than 0.01, respectively). Although the auto MLR of the lymphadenopathy patients rose to control values with the addition of exogenous IL-2, the auto MLR of the AIDS patients did not (P less than 0.01). This lack of responsiveness to IL-2 in the AIDS group was due to their inability to generate IL-2 receptors as shown by the absence of IL-2 absorption by activated cells and the absence of the Tac antigen (IL-2 receptor) on these same cells. The T4+ and T8+ T-cell subsets from the AIDS patients each demonstrated depressed IL-2 production and responsiveness following activation with autologous cells or mitogen, as well as the absence of Tac antigen. The diminished T-cell proliferation in the auto MLR in the lymphadenopathy group is associated with one defect, low IL-2 production, while the depressed proliferation in the AIDS group is associated with two defects, low IL-2 production and a lack of IL-2 receptor generation. These studies demonstrate that IL-2 receptor generation helps distinguish homosexuals with lymphadenopathy from those with AIDS, and that in addition to T-cell defects in the OKT4+ T-cell subset there are significant abnormalities in the OKT8+ T-cell subset in AIDS patients.
获得性免疫缺陷综合征(艾滋病)是一种主要在同性恋男性中发现的疾病,由机会性感染和肿瘤组成,是由于获得性T细胞缺陷所致。在本报告中,我们研究了各种T细胞功能,这些功能可能有助于区分有包括淋巴结病在内的症状复合体的同性恋者和患有艾滋病的同性恋者。与健康的同性恋者或异性恋对照相比,淋巴结病患者和艾滋病患者的T淋巴细胞在自体(自身)和异体(同种异体)混合淋巴细胞反应(MLR)中的增殖反应明显降低(P小于0.001)。由于MLR中的增殖依赖于白细胞介素2(IL-2),一种T细胞生长因子,我们研究了不同组同性恋者和异性恋对照中IL-2的产生和对IL-2的反应。与健康的同性恋者或异性恋对照(均为5.0 U/ml)相比,淋巴结病患者和艾滋病患者的IL-2产生明显降低,分别为1.0和0.1 U/ml(分别为P小于0.05和P小于0.01)。尽管添加外源性IL-2后淋巴结病患者的自身MLR升至对照值,但艾滋病患者的自身MLR并未升高(P小于0.01)。艾滋病组对IL-2缺乏反应是由于他们无法产生IL-2受体,这表现为活化细胞不吸收IL-2以及这些相同细胞上不存在Tac抗原(IL-2受体)。艾滋病患者的T4+和T8+ T细胞亚群在用自体细胞或有丝分裂原激活后,各自表现出IL-2产生和反应降低,以及不存在Tac抗原。淋巴结病组自身MLR中T细胞增殖减少与一个缺陷相关,即IL-2产生低,而艾滋病组增殖降低与两个缺陷相关,即IL-2产生低和缺乏IL-2受体生成。这些研究表明,IL-2受体生成有助于区分有淋巴结病的同性恋者和患有艾滋病的同性恋者,并且除了OKT4+ T细胞亚群中的T细胞缺陷外,艾滋病患者的OKT8+ T细胞亚群也存在明显异常。