The regulation of dendritic cell function by calcium-signaling and its inhibition by microbial pathogens

被引：41

作者：

Connolly, S. F.

Kusner, D. J. ^{[1
]}

机构：

[1] Univ Iowa, Div Infect Dis, Dept Internal Med, Iowa City, IA 52242 USA

[2] Univ Iowa, Grad Program Immunol, Dept Med, Iowa City, IA 52242 USA

来源：

IMMUNOLOGIC RESEARCH | 2007年 / 39卷 / 1-3期

关键词：

calmodulin; phagosome; macrophage; Ca2+/calmodulin protein kinase II; Mycobacterium tuberculosis; innate immunity; antigen presentation; MHC class II; signal transduction; infectious disease;

D O I：

10.1007/s12026-007-0076-1

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

Dendritic cells (DC) are the sentinels of the immune system, linking innate with adaptive responses. The functional responses of DC are subject to complex regulation and serve as targets for pathogens. Ca2+-mediated signal transduction pathways serve a central regulatory role in DC responses to diverse antigens, including TLR ligands, intact bacteria, and microbial toxins. This review summarizes the major mechanisms of Ca2+-signaling that DC utilize to regulate maturation and antigen presentation, including a Ca2+-calmodulin (CaM)-CaM kinase II pathway that is localized to phagosomes and is targeted by the human intracellular pathogen, Mycobacterium tuberculosis. Restoration of functional Ca2+ signaling in DC may provide a novel mechanism to enhance therapy and promote vaccine efficacy to infectious diseases, including tuberculosis.

引用

页码：115 / 127

页数：13

共 64 条

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