Freedman D O, Nutman T B, Jamal S, Kumaraswami V, Ottesen E A
Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, Bethesda, MD 20892.
J Immunol. 1989 Jan 15;142(2):653-8.
Local host immune responses to the lymphatic-dwelling filarial parasite Wuchereria bancrofti are important in the pathogenesis of the lymphangitis that leads to filarial elephantiasis. That the lymphatic endothelial cells may be important in this inflammatory process was shown by the ability of supernatants generated from filarial Ag-driven PBMC of individuals with filarial elephantiasis caused by W. bancrofti infection to up-regulate class I MHC expression on human umbilical vein endothelial cells when compared to unstimulated control supernatants from the same individual (relative fluorescence intensity = 159% +/- 13.5; p less than 0.001). In contrast, individuals with the same filarial infection but manifesting no lymphatic disease were unable to generate, in response to filarial Ag the cytokines required for this activation (relative fluorescence intensity = 93% +/- 2.6). Supernatants induced by a non-filarial Ag (purified protein derivative) were able to effect class I MHC up-regulation in both patient groups. The same filarial Ag-driven supernatants did not cause detectable class II MHC staining on human umbilical vein endothelial cells. These results suggest a likely role for parasite Ag-driven, cytokine-mediated endothelial cell activation in the pathogenesis of lymphatic inflammatory/obstructive filarial disease.
局部宿主对寄生于淋巴管的丝虫寄生虫班氏吴策线虫的免疫反应在导致丝虫象皮肿的淋巴管炎发病机制中起重要作用。由感染班氏吴策线虫引起丝虫象皮肿的个体的丝虫抗原驱动的外周血单核细胞产生的上清液，与来自同一个体的未刺激对照上清液相比，能够上调人脐静脉内皮细胞上的I类主要组织相容性复合体（MHC）表达，这表明淋巴管内皮细胞在这一炎症过程中可能很重要（相对荧光强度 = 159% ± 13.5；p < 0.001）。相比之下，患有相同丝虫感染但未表现出淋巴疾病的个体，在接触丝虫抗原后无法产生这种激活所需的细胞因子（相对荧光强度 = 93% ± 2.6）。由非丝虫抗原（纯化蛋白衍生物）诱导的上清液能够在两个患者组中上调I类MHC表达。相同的丝虫抗原驱动的上清液在人脐静脉内皮细胞上未引起可检测到的II类MHC染色。这些结果表明，寄生虫抗原驱动的、细胞因子介导的内皮细胞激活在淋巴炎性/阻塞性丝虫病的发病机制中可能起作用。
