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Antibody-mediated killing of suppressor T lymphocytes as a possible cause of macroglobulinemia in the tropical splenomegaly syndrome.

机译:抗体介导的抑制性T淋巴细胞杀伤可能是热带脾肿大综合征中巨球蛋白血症的可能原因。

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摘要

To investigate the pathogenesis of macroglobulinemia in the tropical splenomegaly syndrome (TSS), we assessed the functional activity of B lymphocytes and T cell subsets in a pokeweed mitogen-driven assay of immunoglobulin synthesis. Mononuclear cells from patients with TSS produced more IgM than cells from village or from distant controls. This appeared to result from a decrease in the number and/or activity of suppressor T cells of the T8+ phenotype. The lack of functional suppressor T lymphocytes was associated with the presence in sera from patients with TSS of IgM antibodies that specifically killed T8+, 9.3-, 60.1+ T cells from normal donors. These results support the hypothesis that macroglobulinemia in TSS results from defective immunoregulatory control of B cell function, and that this may be caused by lysis of suppressor T cells by specific lymphocytotoxic antibodies produced by patients with this syndrome.
机译:为了调查热带脾肿大综合征(TSS)中大球蛋白血症的发病机理,我们在商陆有丝分裂原促分裂的免疫球蛋白合成测定中评估了B淋巴细胞和T细胞亚群的功能活性。 TSS患者的单核细胞产生的IgM高于乡村或远距离对照者的细胞。这似乎是由于T8 +表型的抑制性T细胞的数量和/或活性降低引起的。功能抑制性T淋巴细胞的缺乏与IgM抗体的TSS患者血清中的存在有关,该IgM抗体特异性杀死了正常供体的T8 +,9.3-,60.1 + T细胞。这些结果支持以下假设:TSS中的巨球蛋白血症是由B细胞功能的免疫调节控制缺陷引起的,并且这可能是由于该综合征患者产生的特定淋巴细胞毒性抗体对抑制性T细胞的溶解引起的。

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