Afonso L C, Scott P
Department of Pathobiology, School of Veterinary Medicine, University of Pennsylvania, Philadelphia 19104.
Infect Immun. 1993 Jul;61(7):2952-9. doi: 10.1128/iai.61.7.2952-2959.1993.
Leishmaniae are protozoans which, depending upon both the host and parasite species, can cause either a healing or nonhealing infection. While C57BL/10 mice are able to heal following infection with Leishmania major, they fail to heal following infection with Leishmania amazonensis. In order to address the role of Th1 and Th2 cell responses in the outcome of these infections in C57BL/10 mice, gamma interferon (IFN-gamma) and interleukin-4 (IL-4) production was assessed. While cells from L. major-infected C57BL/10 mice produced high levels of IFN-gamma, cells from L. amazonensis-infected animals produced little or no IFN-gamma. On the other hand, IL-4 was produced only by cells from L. amazonensis-infected C57BL/10 mice, but this production was restricted to the first few weeks of infection. Later in infection, when lesions were evident, no IL-4 was detected. Treatment of BALB/c mice with a monoclonal antibody (11B11) directed against IL-4 induced a dramatic reduction in L. amazonensis lesions. This reduction was associated with a decrease in IL-4 levels and an increase in IFN-gamma production. However, only a slight reduction in lesion sizes and parasite numbers was observed when anti-IL-4-treated C57BL/10 mice were infected with L. amazonensis. These results suggest that IL-4 may have an important role in mediating susceptibility to L. amazonensis in BALB/c mice, as previously demonstrated for L. major. More importantly, however, the data suggest that susceptibility to L. amazonensis in C57BL/10 mice is due to the absence of a Th1 cell response, rather than to the presence of a Th2 cell response.
利什曼原虫是一种原生动物，根据宿主和寄生虫的种类不同，可导致感染愈合或不愈合。虽然C57BL/10小鼠感染硕大利什曼原虫后能够自愈，但感染亚马逊利什曼原虫后却无法自愈。为了研究Th1和Th2细胞反应在C57BL/10小鼠这些感染结果中的作用，对γ干扰素（IFN-γ）和白细胞介素-4（IL-4）的产生进行了评估。来自感染硕大利什曼原虫的C57BL/10小鼠的细胞产生高水平的IFN-γ，而来自感染亚马逊利什曼原虫的动物的细胞产生很少或不产生IFN-γ。另一方面，只有来自感染亚马逊利什曼原虫的C57BL/10小鼠的细胞产生IL-4，但这种产生仅限于感染的最初几周。在感染后期，当病变明显时，未检测到IL-4。用针对IL-4的单克隆抗体（11B11）治疗BALB/c小鼠，可使亚马逊利什曼原虫病变显著减少。这种减少与IL-4水平的降低和IFN-γ产生的增加有关。然而，当用抗IL-4处理的C57BL/10小鼠感染亚马逊利什曼原虫时，仅观察到病变大小和寄生虫数量略有减少。这些结果表明，IL-4可能在介导BALB/c小鼠对亚马逊利什曼原虫的易感性方面起重要作用，正如先前对硕大利什曼原虫所证明的那样。然而，更重要的是，数据表明C57BL/10小鼠对亚马逊利什曼原虫的易感性是由于缺乏Th1细胞反应，而不是由于存在Th2细胞反应。
