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肿瘤坏死因子α在抗微小隐孢子虫感染免疫发育中的作用。

Role of tumor necrosis factor alpha in development of immunity against Cryptosporidium parvum infection.

作者信息

Lean I-Sarah, Lacroix-Lamandé Sonia, Laurent Fabrice, McDonald Vincent

机构信息

Barts and the London School of Medicine, Institute of Cell and Molecular Science, Centre for Gastroenterology, Turner Street, London E1 2AD, United Kingdom.

出版信息

Infect Immun. 2006 Jul;74(7):4379-82. doi: 10.1128/IAI.00195-06.

DOI:10.1128/IAI.00195-06
PMID:16790816
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1489749/
Abstract

Tumor necrosis factor (TNF-alpha) significantly reduced Cryptosporidium parvum development in a murine enterocyte cell line, and a key mechanism of action appeared to be inhibition of parasite invasion. However, TNF-alpha-deficient mice controlled infection as effectively as wild-type mice. This suggests that TNF-alpha might have only a redundant role for establishing immunity against C. parvum.

摘要

肿瘤坏死因子（TNF-α）显著降低了小鼠肠上皮细胞系中小隐孢子虫的发育，其关键作用机制似乎是抑制寄生虫入侵。然而，TNF-α基因缺陷型小鼠控制感染的效果与野生型小鼠一样有效。这表明TNF-α在建立针对小隐孢子虫的免疫方面可能仅起冗余作用。

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本文引用的文献

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Cryptosporidium parvum-specific CD4 Th1 cells from sensitized donors responding to both fractionated and recombinant antigenic proteins.来自致敏供体的对分级分离和重组抗原蛋白均有反应的微小隐孢子虫特异性CD4 Th1细胞。
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TNF-alpha is a critical negative regulator of type 1 immune activation during intracellular bacterial infection.肿瘤坏死因子-α是细胞内细菌感染期间1型免疫激活的关键负调节因子。
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Interleukin-4 and transforming growth factor beta have opposing regulatory effects on gamma interferon-mediated inhibition of Cryptosporidium parvum reproduction.白细胞介素-4和转化生长因子β对γ干扰素介导的微小隐孢子虫繁殖抑制具有相反的调节作用。
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