Iron metabolism and the innate immune response to infection

被引：175
|
作者：
Johnson, Erin E. [2 ]
Wessling-Resnick, Marianne [1 ]
机构：
[1] Harvard Univ, Sch Publ Hlth, Dept Genet & Complex Dis, Boston, MA 02115 USA
[2] John Carroll Univ, Dept Biol, University Hts, OH 44118 USA
来源：
MICROBES AND INFECTION | 2012年 / 14卷 / 03期
关键词：
Innate immunity; Inflammation; Hepcidin; HEMOCHROMATOSIS PROTEIN HFE; MYCOBACTERIUM-TUBERCULOSIS; TRYPANOSOMA-CRUZI; TRANSFERRIN RECEPTOR; INTRACELLULAR GROWTH; CHELATOR DESFERRIOXAMINE; INCREASED SUSCEPTIBILITY; HEME OXYGENASE-1; OXIDATIVE BURST; EARLY ENDOSOMES;
D O I：
10.1016/j.micinf.2011.10.001
中图分类号：
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号：
100102 ;
摘要：
Host antimicrobial mechanisms reduce iron availability to pathogens. Iron proteins influencing the innate immune response include hepcidin, lactoferrin, siderocalin, haptoglobin, hemopexin, Nrampl, ferroportin and the transferrin receptor. Numerous global health threats are influenced by iron status and provide examples of our growing understanding of the connections between infection and iron metabolism. (C) 2011 Institut Pasteur. Published by Elsevier Masson SAS. All rights reserved.
引用
收藏
页码：207 / 216
页数：10
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