The role of As60A, a TGF-β homolog, in Anopheles stephensi innate immunity and defense against Plasmodium infection

被引：19

作者：

Crampton, Andrea ^{[1
]}

Luckhart, Shirley ^{[1
]}

机构：

[1] Virginia Tech, Dept Biochem, Blacksburg, VA 24061 USA

来源：

INFECTION GENETICS AND EVOLUTION | 2001年 / 1卷 / 02期

基金：

美国国家卫生研究院;

关键词：

As60A; Malaria; Mosquito; Transforming growth factor beta (TGF-beta); Innate immunity; Plasmodium;

D O I：

10.1016/S1567-1348(01)00017-X

中图分类号：

R51 [传染病];

学科分类号：

100401 ;

摘要：

We have examined the constitutive and induced expression of As60A in Anopheles stephensi females. As60A is expressed throughout the body of A. stephensi, including the midgut, fat body and developing eggs. We discovered that As60A is induced in the midgut and carcass of A. stephensi in response to Plasmodium infection. Induction of As60A correlates with periods of parasite motility and reproduction. Further, induction is dependent on the intensity of parasite infection: low numbers of parasites do not induce As60A expression. Thus, we conclude that As60A is a component of the A. stephensi immune response to Plasmodium infection. The involvement of a member of the transforming growth factor beta (TGF-beta) super family in the mosquito immune response is analogous to the involvement of TGF-beta 1 in the mammalian immune response to Plasmodium. The modulation of As60A and A. stephensi nitric oxide synthase (AsNOS) expression in response to Plasmodium indicates that homologs of effector (NOS) and regulator (TGF-beta 1) gene super families may defend evolutionarily diverse hosts against a shared pathogen. (C) 2001 Science B.V. All rights reserved.

引用

页码：131 / 141

页数：11

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