Raziuddin S, Telmasani A W, el-Hag el-Awad M, al-Amari O, al-Janadi M
Department of Clinical Immunology, King Saud University, College of Medicine, Abha, Saudi Arabia.
Eur J Immunol. 1992 May;22(5):1143-8. doi: 10.1002/eji.1830220506.
Visceral leishmaniasis (VL) caused by Leishmania donovani, a protozoan parasite, is a disease of high morbidity associated with hepatosplenomegaly, hypergammaglobulinemia, fever and death. One of the immunological hallmarks of VL is a remarkable increase in serum immunoglobulin levels as a result of polyclonal B cell activation. This study demonstrated that T lymphocytes expressing the T cell receptors (TcR) gamma delta in association with CD3 molecules are increased in circulation of patients with VL. A large proportions of TcR gamma delta-bearing T cells had CD4+ CD8- phenotype, and expressed CD25, CD38, CD71 and HLA-DR activation antigens. Furthermore, we demonstrated wide functional differences in TcR gamma delta and TcR alpha beta T cells in their proliferative response, secretion of interleukin-2 (IL-2), B cell growth factor (BCGF) and B cell differentiation factor (BCDF). It was of interest that the TcR gamma delta T cells from patients with VL could be expanded by in vitro culture with human recombinant IL-2. Although these TcR gamma delta T cells secreted diminished levels of IL-2, they produced highly augmented levels of both BCGF and BCDF, suggesting that secretion of these lymphokines in these T cell subsets is regulated independently. The relative increases in the CD4+ CDw29+ TcR gamma delta T cell subsets and their secretion of highly elevated levels of BCGF and BCDF largely accounted for the humoral immune system abnormality and hypergammaglobulinemia found in this disease. These observations may help to explain that TcR gamma delta T cells might be functional in vivo and are involved in immunological mechanisms of pathogenesis in VL.
由原生动物寄生虫杜氏利什曼原虫引起的内脏利什曼病（VL）是一种高发病率疾病，与肝脾肿大、高球蛋白血症、发热及死亡相关。VL的免疫特征之一是多克隆B细胞活化导致血清免疫球蛋白水平显著升高。本研究表明，表达与CD3分子相关的T细胞受体（TcR）γδ的T淋巴细胞在VL患者循环中增多。大部分携带TcRγδ的T细胞具有CD4 + CD8 - 表型，并表达CD25、CD38、CD71和HLA - DR活化抗原。此外，我们证明了TcRγδ和TcRαβ T细胞在增殖反应、白细胞介素 - 2（IL - 2）、B细胞生长因子（BCGF）和B细胞分化因子（BCDF）分泌方面存在广泛的功能差异。有趣的是，VL患者的TcRγδ T细胞可通过用人重组IL - 2进行体外培养而扩增。尽管这些TcRγδ T细胞分泌的IL - 2水平降低，但它们产生的BCGF和BCDF水平却显著升高，这表明这些T细胞亚群中这些淋巴因子的分泌是独立调节的。CD4 + CDw29 + TcRγδ T细胞亚群的相对增加及其分泌的高水平BCGF和BCDF在很大程度上解释了该疾病中发现的体液免疫系统异常和高球蛋白血症。这些观察结果可能有助于解释TcRγδ T细胞在体内可能具有功能，并参与了VL发病机制的免疫机制。
