Piessens W F, Hoffman S L, Wadee A A, Piessens P W, Ratiwayanto S, Kurniawan L, Campbell J R, Marwoto H A, Laughlin L L
J Clin Invest. 1985 Jun;75(6):1821-7. doi: 10.1172/JCI111895.
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.
为了研究热带脾肿大综合征（TSS）中巨球蛋白血症的发病机制，我们在商陆有丝分裂原驱动的免疫球蛋白合成试验中评估了B淋巴细胞和T细胞亚群的功能活性。TSS患者的单核细胞比来自村庄或远处对照的细胞产生更多的IgM。这似乎是由于T8 +表型的抑制性T细胞数量和/或活性降低所致。功能性抑制性T淋巴细胞的缺乏与TSS患者血清中存在特异性杀死正常供体的T8 +、9.3 -、60.1 + T细胞的IgM抗体有关。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，这可能是由该综合征患者产生的特异性淋巴细胞毒性抗体裂解抑制性T细胞所致。
