Okudaira K, Searles R P, Tanimoto K, Horiuchi Y, Williams R C
J Clin Invest. 1982 Apr;69(4):1026-38. doi: 10.1172/jci110506.
Systemic lupus erythematosus (SLE) is an autoimmune disease with multiple immune disturbances whose mechanisms remain unclear. We examined the interaction of antilymphocyte antibodies with cultured normal T lymphocytes. T cells were prepared by E-rosetting after petri-dish removal of adherent cells and cultured for 2-7 d in the presence of SLE sera or normal human sera. Cultured T cells were washed and sonicated, and the amount of cell-associated IgG was quantitated by radioimmunoassay or enzyme-linked immunoassay (ELISA) methods. T cells cultured with 27 of 39 SLE sera showed marked increments of associated immunoglobulin G (IgG) although this was not observed with sera from mixed connective tissue disease patients containing high titers of ribonucleoprotein antibody or normal donors. The effective factors for IgG association in SLE sera were absorbed with normal peripheral blood lymphocytes or T cells. Anti-T cell IgG cytotoxic activity strongly correlated with T cell IgG association (P less than 0.01). T cell-associated IgG was not removed by stripping of cell membrane IgG from living cells by acid buffer treatment; indirect immunofluorescence of cells fixed after 2-4 d of culture revealed cytoplasmic IgG staining. IgG anti-T cell antibodies appeared to associate inside the cell membrane or to penetrate into the cytoplasm of cells. T cell Fc receptor blocking by heat-aggregated IgG or anti-beta 2-microglobulin antibody did not alter IgG cell association. Since pepsin-digested SLE sera showed no T cell association activity, whole IgG antibody molecules appeared to be necessary for interaction with cultured T cells. In addition, reduction and alkylation of active SLE sera completely nullified T cell reactivity. When normal T cells were cultured with SLE sera showing marked IgG T cell association, viability of cultured T cells decreased rapidly after 4 d, which suggests that IgG anti-T cell antibodies were associated with cell destruction. IgG cell-associating antilymphocyte antibodies present in SLE sera may cause T cell disturbances in vivo and may be related to the lymphocytopenia present in SLE patients.
系统性红斑狼疮（SLE）是一种存在多种免疫紊乱的自身免疫性疾病，其发病机制尚不清楚。我们研究了抗淋巴细胞抗体与培养的正常T淋巴细胞之间的相互作用。通过在培养皿中去除贴壁细胞后进行E花环形成制备T细胞，并在SLE血清或正常人血清存在的情况下培养2 - 7天。培养的T细胞经洗涤和超声处理后，通过放射免疫测定法或酶联免疫吸附测定（ELISA）方法对细胞相关IgG的量进行定量。用39份SLE血清中的27份培养的T细胞显示相关免疫球蛋白G（IgG）显著增加，而在含有高滴度核糖核蛋白抗体的混合性结缔组织病患者血清或正常供体血清中未观察到这种情况。SLE血清中与IgG结合的有效因子可被正常外周血淋巴细胞或T细胞吸收。抗T细胞IgG细胞毒性活性与T细胞IgG结合密切相关（P小于0.01）。通过酸性缓冲液处理从活细胞中去除细胞膜IgG并不能去除T细胞相关IgG；培养2 - 4天后固定细胞的间接免疫荧光显示细胞质IgG染色。IgG抗T细胞抗体似乎在细胞膜内结合或穿透到细胞细胞质中。热聚集IgG或抗β2 - 微球蛋白抗体阻断T细胞Fc受体并不会改变IgG与细胞的结合。由于胃蛋白酶消化的SLE血清未显示T细胞结合活性，完整的IgG抗体分子似乎是与培养的T细胞相互作用所必需的。此外，活性SLE血清的还原和烷基化完全消除了T细胞反应性。当正常T细胞与显示显著IgG T细胞结合的SLE血清一起培养时，培养的T细胞在4天后活力迅速下降，这表明IgG抗T细胞抗体与细胞破坏有关。SLE血清中存在的与细胞结合的IgG抗淋巴细胞抗体可能在体内导致T细胞紊乱，并且可能与SLE患者中存在的淋巴细胞减少有关。
