T cells facilitate Brugia malayi development in TCRαnull mice
T cells facilitate Brugia malayi development in TCRαnull mice
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DOI：
10.1006/expr.1999.4438
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发表时间：
1999-09-01
影响因子：
2.1
通讯作者：
Rajan, TV
中科院分区：
文献类型：
--
作者：
Babu, S;Shultz, LD;Rajan, TV
巴布，S.，舒尔茨湖D、和Rajan，T.五. 1999年。T细胞促进TCR α（无效）小鼠中马来丝虫的发育。实验寄生虫学93，55-57。马来丝虫在小鼠体内的宿主-寄生虫相互作用是复杂和多因素的。为了研究T细胞在早期B。在Malayi发展中，我们感染了TCR α（null）小鼠，其保留了CD 4（+）TCR β（+）细胞的群体和TCR β（null）小鼠，其缺乏所有TCR α β（+）T细胞。TCR α（null）小鼠允许L4幼虫和成虫发育，但TCR β（null）小鼠不允许。前者中CD 4（+）T细胞的耗尽废除了容许表型。似乎在TCR α（null）小鼠中描述的CD 4（+）TCR β（+）T细胞可能促进早期B。马来发展。这些数据与我们先前证明的NK细胞在促进SCID小鼠蠕虫生长中的作用相似。(C)北京：科学出版社.
Babu, S., Shultz, L. D., and Rajan, T. V. 1999. T cells facilitate Brugia malayi development in TCR alpha(null) mice. Experimental Parasitology 93, 55-57. The host-parasite interactions of Brugia malayi in mice are complex and multifactorial. In order to study the role of T cells in early B. malayi development, we infected TCR alpha(null) mice, which retain a population of CD4(+) TCR beta(+) cells and TCR beta(null) mice, which lack all TCR alpha beta(+) T cells. TCR alpha(null) mice were permissive to L4 larval and adult worm development but TCR beta(null) mice were not. Depletion of the CD4(+) T cells in the former abrogated the permissive phenotype. It appears that the CD4(+) TCR beta(+) T cells that have been described in TCR alpha(null) mice may facilitate early B. malayi development. These data are similar to our earlier demonstration of the role of NK cells in facilitating worm growth in SCID mice. (C) 1999 Academic Press.