Aguilar-Torrentera F, Carlier Y
Departamento de Inmunología, Escuela Nacional de Ciencias Biológicas, IPN, México DF.
Rev Latinoam Microbiol. 2001 Jul-Sep;43(3):135-42.
Infection with Leishmania sp. is particularly suitable for the study of immunoregulatory mechanisms associated with host susceptibility or resistance. The clinical spectrum of this infection results from parasite virulence factors and host immune responses, some of which acting in a host protective manner while others exacerbate the disease. In the mouse model, factors governing resistance to Leishmania major infection mainly depends on the IFN-gamma activation of the leishmanicidal function of macrophages, and the Fas/ FasL-dependent T-cell cytotoxicity against infected macrophages. On the other hand, the immunological factors of susceptibility involve: I) the early upregulation of IL-4 production induced by the LACK antigen, II) the upregulation of IL-2 production, III) the high production of TGF-beta as macrophage deactivating factor, and IV) the production of IL-10 by the L. major infected macrophages, inhibited their microbicidal activity.
感染利什曼原虫特别适合用于研究与宿主易感性或抵抗力相关的免疫调节机制。这种感染的临床谱由寄生虫毒力因子和宿主免疫反应导致，其中一些以宿主保护方式起作用，而另一些则会加重疾病。在小鼠模型中，控制对硕大利什曼原虫感染抵抗力的因素主要取决于巨噬细胞杀利什曼原虫功能的IFN-γ激活，以及Fas/FasL依赖性T细胞对感染巨噬细胞的细胞毒性。另一方面，易感性的免疫因素包括：I）LACK抗原诱导的IL-4产生的早期上调，II）IL-2产生的上调，III）作为巨噬细胞失活因子的TGF-β的高产生，以及IV）被硕大利什曼原虫感染的巨噬细胞产生的IL-10抑制了它们的杀菌活性。
