Interferon-γ is required for innate immunity to Cryptosporidium parvum in mice
Interferon-γ is required for innate immunity to Cryptosporidium parvum in mice
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DOI：
10.1086/315802
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发表时间：
2000-09-01
影响因子：
6.4
通讯作者：
Cosyns, M
中科院分区：
文献类型：
--
作者：
Hayward, AR;Chmura, K;Cosyns, M
虽然从隐孢子虫感染中恢复需要CD4T细胞，但患有严重联合免疫缺陷(SCID)的小鼠仍然长期感染，没有不良影响。相比之下，使用干扰素(干扰素)-γ的能力受到中和或基因敲除影响的小鼠，会经历严重的隐孢子虫感染，可能会导致死亡。为了确定SCID小鼠对微小隐孢子虫(CP)的天然免疫是否需要干扰素-γ，培育了双免疫缺陷C57BL/6SCID-干扰素-γ基因敲除小鼠。这些小鼠经历了严重的肠道CP感染；与仅携带SCID突变的小鼠或仅携带中断的干扰素-伽马基因的小鼠相比，死亡或死亡的人数要多得多。诱导型一氧化氮合酶或Fas/Fas配体基因突变的小鼠从肺炎衣原体感染中恢复正常。结果表明，由于SCID突变而无法产生特异性免疫反应的小鼠，在感染CP后需要干扰素-γ来避免死亡。
Although CD4 T cells are required for recovery from cryptosporidial infection, mice with severe combined immunodeficiency (SCID) remain infected for long periods without ill effect. In contrast, mice whose ability to use interferon(IFN)-gamma is impaired, by neutralization or gene knockout, experience heavy cryptosporidial infection that may lead to death. To determine whether the innate immunity of SCID mice to Cryptosporidium parvum (CP) requires IFN-gamma, doubly immunodeficient C57BL/6 SCID-IFN-gamma knockout mice were bred. These mice experienced heavy CP infections of the gut; a significantly greater number became moribund or died, compared with mice carrying the SCID mutation alone or carrying disrupted IFN-gamma genes alone. Mice with gene disruptions of inducible nitric oxide synthetase or Fas/Fas ligand recovered normally from CP infection. The results indicate that mice unable to produce specific immune responses because of the SCID mutation require IFN-gamma to avoid death after infection with CP.