IMMUNE-RESPONSES ASSOCIATED WITH SUSCEPTIBILITY OF C57BL/10 MICE TO LEISHMANIA-AMAZONENSIS
IMMUNE-RESPONSES ASSOCIATED WITH SUSCEPTIBILITY OF C57BL/10 MICE TO LEISHMANIA-AMAZONENSIS
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DOI：
10.1128/iai.61.7.2952-2959.1993
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发表时间：
1993-07-01
影响因子：
3.1
通讯作者：
SCOTT, P
中科院分区：
文献类型：
--
作者：
AFONSO, LCC;SCOTT, P
利什曼原虫是原生动物，根据宿主和寄生虫的种类，可以引起愈合或不愈合的感染。虽然C57 BL/10小鼠能够在感染硕大利什曼原虫后愈合，但它们在感染亚马逊利什曼原虫后未能愈合。为了阐明Th 1和Th 2细胞应答在C57 BL/10小鼠中这些感染的结果中的作用，评估了γ干扰素（IFN-γ）和白细胞介素-4（IL-4）的产生。L.主要感染的C57 BL/10小鼠产生高水平的来自L.感染亚马逊河原虫的动物产生很少或不产生EFN-γ。IL-4仅由L.安他唑感染的C57 BL/10小鼠，但这种生产仅限于感染的前几周。在感染后期，当病变明显时，没有检测到IL-4。用抗IL-4的单克隆抗体（11B 11）处理BALB/c小鼠，诱导L.亚马逊损伤这种减少与IL-4水平的降低和IFN-γ产生的增加有关。然而，当抗IL-4处理的C57 BL/10小鼠感染L.亚马逊河。提示IL-4在介导L.在BALB/c小鼠中，如先前证明的L.少校然而，更重要的是，数据表明，对L。在C57 BL/10小鼠中，亚马逊病毒感染是由于Th 1细胞应答的缺乏，而不是由于Th 2细胞应答的存在。
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 EFN-gamma, cells from L. amazonensis-infected animals produced little or no EFN-gamma. On the other hand, IL-4 was produced only by cells from L. antazonensis-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.