IMMUNOLOGICAL STUDIES IN THE ACQUIRED-IMMUNODEFICIENCY-SYNDROME .2. ACTIVE SUPPRESSION OR INTRINSIC DEFECT - INVESTIGATED BY MIXING AIDS CELLS WITH HLA-DR IDENTICAL NORMAL-CELLS
IMMUNOLOGICAL STUDIES IN THE ACQUIRED-IMMUNODEFICIENCY-SYNDROME .2. ACTIVE SUPPRESSION OR INTRINSIC DEFECT - INVESTIGATED BY MIXING AIDS CELLS WITH HLA-DR IDENTICAL NORMAL-CELLS
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DOI：
10.1111/j.1365-3083.1986.tb02003.x
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发表时间：
1986-06-01
影响因子：
3.7
通讯作者：
SVEJGAARD, A
中科院分区：
文献类型：
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作者：
HOFMANN, B;ODUM, N;SVEJGAARD, A
本文研究了6例获得性免疫缺陷综合征（AIDS）患者和6例健康对照的淋巴细胞对丝裂原(植物血凝素（PHA）、豆豆蛋白A （Con A）和美洲商陆丝裂原（PWM）、异体细胞和抗原纯化蛋白衍生物（PPD）的转化反应。6例健康对照均与1例艾滋病患者的HLA-DR和混合淋巴细胞培养（MLC）相同。将辐照或未辐照的艾滋病外周血单个核细胞（PBMC）添加到受强丝裂原PHA和Con A或同种异体细胞刺激的健康对照hla - dr相同的PMBC培养物中，没有观察到抑制的证据，但抑制可能与PWM或PPD刺激的培养物反应降低有关。添加艾滋病细胞巨量培养的上清液不抑制对照PBMC的反应。因此，任何淋巴细胞亚群或可溶性因子的单独抑制都不能解释艾滋病中普遍严重抑制的转化反应。在有丝分裂原刺激的艾滋病PBMC和某些抗原或同种异体细胞刺激的艾滋病PBMC培养物中，加入来自健康对照或这些培养物的上清液，会增加反应，其程度与添加商业获得的t细胞生长因子（TCGF）后所见的相同。这表明艾滋病细胞缺乏产生TCGF。重度辐照的艾滋病PBMC能够恢复对纯化的hla - dr相同的正常T细胞的有丝分裂原和抗原的转化反应，这表明艾滋病细胞具有正常的抗原提呈能力和白细胞介素（IL-1）的产生。然而，在MLC中，艾滋病PBMC对正常PBMC的刺激能力非常差。总之，我们的实验表明，艾滋病细胞的免疫缺陷可能部分是由于T淋巴细胞产生TCGF的能力下降，树突状细胞的数量和/或功能也可能减少。
The lymphocyte transformation responses to mitogens (phytohaemagglutinin (PHA), concanavalin A (Con A), and pokeweed mitogen (PWM)), allogeneic cells, and the antigen-purified protein derivative (PPD) were studied in six acquired immunodeficiency syndrome (AIDS) patients and in six healthy controls, each of whom was HLA-DR- and mixed lymphocyte culture (MLC)-identical with one of the AIDS patients. No evidence of suppression was observed when irradiated or non-irradiated AIDS peripheral blood mononuclear cells (PBMC) were added to cultures of HLA-DR-identical PMBC from healthy controls stimulated with the strong mitogens PHA and Con A or with allogeneic cells, but suppression may be involved in the decreased responses in cultures stimulated with PWM or PPD. Addition of supernatants from macrocultures of AIDS cells did not suppress responses of control PBMC. Thus, suppression by any lymphocyte subset or soluble factor alone cannot explain the generally severely depressed transformation responses in AIDS. Addition of heavily irradiated HLA-DR-identical PBMC from healthy controls or supernatants from these cultures led to increased responses in cultures of mitogen-stimulated AIDS PBMC and in some cultures of antigen or allogeneic cell-stimulated AIDS PBMC, which were of the same magnitude as seen after the addition of commercially obtained T-cell growth factor (TCGF). This indicates that AIDS cells are deficient in producing TCGF. Heavily irradiated AIDS PBMC were capable of restoring the transformation responses to mitogens and antigens of purified HLA-DR-identical normal T cells, indicating that AIDS cells have a normal antigen-presenting capacity and interleukin (IL-1) production. However, AIDS PBMC had a very poor capacity to stimulate normal PBMC in MLC. Together, our experiments suggest that the immune deficiency in AIDS cells may be partially due to a decreased capability of T lymphocytes to produce TCGF and that a decreased number and/or function of dendritic cells may also be involved.