期刊
TRENDS IN IMMUNOLOGY
卷 30, 期 10, 页码 475-487出版社
ELSEVIER SCI LTD
DOI: 10.1016/j.it.2009.07.009
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资金
- Biomedical Research Council
- Agency for Science, Technology and Research (A*STAR)
- Fondos Investigacion Sanitaria
- Ministerio de Ciencia e Innovacion
- Fundacion Mutua Madrilefia de Automovilistica
Prior exposure of innate immune cells like monocytes/macrophages to minute amounts of endotoxin cause them to become refractory to subsequent endotoxin challenge, a phenomenon called endotoxin tolerance. Clinically, this state is associated with monocytes/macrophages in sepsis patients where they contribute to immunosuppression and mortality. The molecular mechanisms underlying endotoxin tolerance remain elusive. The recent appreciation of inflammation as a self-regulating process, the relative contribution of MyD88 versus TRIF signaling pathways in inducing activation or tolerance, plasticity of NF-kappa B function and the role of chromatin modification and microRNAs in LPS-induced gene reprogramming urges a re-evaluation of endotoxin tolerance. This review integrates these new findings into an up-to-date account of endotoxin tolerance, its molecular basis and clinical implications in different pathologies.
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