Gazzinelli R T, Gazzinelli G, Cançado J R, Cardoso J E, Brener Z, Colley D G
Departamento da Bioquimica e Imunologia, Universidade Federal de Minas Gerais, Brazil.
Res Immunol. 1990 Oct;141(8):757-70. doi: 10.1016/0923-2494(90)90006-k.
Patients with chronic Trypanosoma cruzi infections have peripheral auto-anti-idiotype (Id) T cells that proliferate on exposure to immunoaffinity-purified antibodies against T. cruzi epimastigote antigens (EPI). The responses of some patients' (group 1) peripheral blood mononuclear cells (PBMC) to anti-EPI antibodies from sera of patients with the cardiac form of Chagas' disease (Id-C) were inhibited by chloroquine, but responses of other patients' (group 2) PBMC to Id-C were not inhibited. PBMC responses of both group-1 and -2 patients to anti-EPI antibodies from asymptomatic (indeterminate) patients (Id-I) were inhibited by chloroquine, as were their responses to the antigens in EPI. Most patients (69%) in group 1 had indeterminate Chagas' disease, and 100% of the patients in group 2 had severe, cardiac or digestive Chagas' disease. Both the direct (chloroquine-insensitive) and indirect (processed) modes of stimulation by anti-EPI antibodies required adherent cells. In group 2 (direct stimulation), this requirement was met by exogenous IL-1, and neither anti-HLA-DR,DP(DQ) monoclonal antibody (mAb) nor sodium azide inhibited T-cell proliferation. Indirect Id stimulation of group-1 cells by Id-I or Id-C, and group-2 cells by Id-I or EPI, was inhibited by anti-HLA-DR,DP(DQ) mAb or sodium azide, and exogenous IL-1 alone did not support this processed, MHC-mediated T-cell stimulation, but live adherent cells did. The mode of activation of auto-anti-Id T cells from patients with Chagas' disease depends on the clinical form of infection of both the cell donor and the donor of the stimulating anti-EPI antibodies.
患有慢性克氏锥虫感染的患者具有外周自身抗独特型（Id）T细胞，这些T细胞在接触针对克氏锥虫前鞭毛体抗原（EPI）的免疫亲和纯化抗体时会增殖。一些患者（第1组）外周血单核细胞（PBMC）对恰加斯病心脏型患者血清中的抗EPI抗体（Id-C）的反应受到氯喹的抑制，但其他患者（第2组）PBMC对Id-C的反应未受抑制。第1组和第2组患者的PBMC对无症状（不确定型）患者血清中的抗EPI抗体（Id-I）的反应以及对EPI中抗原的反应均受到氯喹的抑制。第1组中的大多数患者（69%）患有不确定型恰加斯病，第2组中的所有患者均患有严重的心脏型或消化型恰加斯病。抗EPI抗体的直接（对氯喹不敏感）和间接（经处理）刺激模式均需要贴壁细胞。在第2组（直接刺激）中，外源性白细胞介素-1满足了这一需求，抗HLA-DR、DP（DQ）单克隆抗体（mAb）和叠氮化钠均未抑制T细胞增殖。Id-I或Id-C对第1组细胞的间接Id刺激以及Id-I或EPI对第2组细胞的间接Id刺激均受到抗HLA-DR、DP（DQ）mAb或叠氮化钠的抑制，单独的外源性白细胞介素-1不支持这种经处理的、MHC介导的T细胞刺激，但活的贴壁细胞可以支持。来自恰加斯病患者的自身抗Id T细胞的激活模式取决于细胞供体和刺激性抗EPI抗体供体的感染临床类型。
