Feng Z Y, Louis J, Kindler V, Pedrazzini T, Eliason J F, Behin R, Vassalli P
WHO-IRTC, University of Lausanne, Epalinges, Switzerland.
Eur J Immunol. 1988 Aug;18(8):1245-51. doi: 10.1002/eji.1830180815.
Previous studies from our laboratory have shown that some in vitro maintained Leishmania major-specific L3T4+ T cells were capable of exacerbating cutaneous leishmaniasis after adoptive transfer to normal syngeneic mice. Results presented in this report show that these cells released substantial amounts of interleukin 3 (IL 3) and granulocyte-macrophage colony-stimulating factors after specific stimulation in vitro. In order to assess the involvement of such lymphokines in the exacerbation of cutaneous leishmaniasis by these L3T4+ T cells, the effect of the administration of important doses of IL 3 on the course of infection with L. major was investigated. The treatment of genetically susceptible BALB/c mice with IL 3 resulted in an enhancement of the size of lesions and favored the multiplication of parasites at anatomical sites distant from the primary lesion. Although IL 3 did not modify the development of lesions in genetically resistant CBA mice, this lymphokine promoted the growth of Leishmania in lymph node draining the lesion. Finally, the addition of IL 3 to macrophages parasitized in vitro enhanced the survival of intracellular Leishmania major.
我们实验室之前的研究表明，一些体外培养的利什曼原虫主要特异性L3T4 + T细胞在过继转移至同基因正常小鼠后能够加剧皮肤利什曼病。本报告中的结果显示，这些细胞在体外特异性刺激后会释放大量白细胞介素3（IL - 3）和粒细胞 - 巨噬细胞集落刺激因子。为了评估此类淋巴因子在这些L3T4 + T细胞加剧皮肤利什曼病过程中的作用，研究了给予大剂量IL - 3对感染利什曼原虫主要种的病程的影响。用IL - 3处理遗传易感的BALB / c小鼠会导致病变大小增加，并有利于寄生虫在远离原发性病变的解剖部位增殖。虽然IL - 3并未改变遗传抗性CBA小鼠病变的发展，但这种淋巴因子促进了病变引流淋巴结中利什曼原虫的生长。最后，向体外被寄生的巨噬细胞中添加IL - 3可提高细胞内利什曼原虫主要种的存活率。
