Hoffman S L, Piessens W F, Ratiwayanto S, Hussein P R, Kurniawan L, Piessens P W, Campbell J R, Marwoto H A
N Engl J Med. 1984 Feb 9;310(6):337-41. doi: 10.1056/NEJM198402093100601.
To study the pathogenesis of tropical splenomegaly syndrome, we compared immunologic findings in patients from Flores, Indonesia, with those obtained in local residents without splenomegaly and in controls. Villagers with tropical splenomegaly syndrome had markedly elevated levels of total IgM, higher titers of IgM antibodies to Plasmodium vivax, and reduced levels of circulating T lymphocytes. The latter were caused by a decrease in the total number of T cells with the suppressor/cytotoxic phenotype (T8+). Levels of B lymphocytes were similar in all groups. All immunologic abnormalities reverted toward normal in patients treated weekly for 9 to 26 months with chloroquine phosphate. These findings suggest that overproduction of immunoglobulins in patients with tropical splenomegaly syndrome is caused by an imbalance in the normal ratio of helper: suppressor T cells that regulate B-lymphocyte function, and that this imbalance is due to a decrease in suppressor T lymphocytes.
为研究热带脾肿大综合征的发病机制,我们比较了印度尼西亚弗洛雷斯岛患者的免疫学检查结果与当地无脾肿大居民及对照组的结果。患有热带脾肿大综合征的村民总IgM水平显著升高,间日疟原虫IgM抗体滴度更高,循环T淋巴细胞水平降低。后者是由具有抑制/细胞毒性表型(T8+)的T细胞总数减少所致。所有组的B淋巴细胞水平相似。用磷酸氯喹每周治疗9至26个月的患者,其所有免疫学异常均恢复正常。这些发现表明,热带脾肿大综合征患者免疫球蛋白的过度产生是由调节B淋巴细胞功能的辅助性T细胞与抑制性T细胞正常比例失衡所致,而这种失衡是由于抑制性T淋巴细胞减少。