期刊
ANNUAL REVIEW OF PATHOLOGY-MECHANISMS OF DISEASE
卷 3, 期 -, 页码 99-126出版社
ANNUAL REVIEWS
DOI: 10.1146/annurev.pathmechdis.3.121806.151456
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资金
- NIAID NIH HHS [R01 AI078287, R01 AI043543, P01 AI057784, R01 AI043543-11A1, R01 AI043543-12] Funding Source: Medline
- NIDDK NIH HHS [P30 DK032520] Funding Source: Medline
- NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [P01AI057784, R01AI078287, R01AI043543] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES [P30DK032520] Funding Source: NIH RePORTER
When cells die in vivo, they trigger an inflammatory response. The ensuing hyperemia, leak of plasma proteins, and recruitment of leukocytes serve a number of useful functions in host defense and tissue repair. However, this response can also cause tissue damage and contribute to the pathogenesis of a number of diseases. Given the key role of inflammation in these processes, it is important to understand the underlying mechanisms that drive this response. Injured cells release danger signals that alert the host to cell death. Some of these molecules are recognized by cellular receptors that stimulate the generation of proinflammatory mediators. Other molecules released by dead cells stimulate the generation of mediators from extracellular sources. The resulting mediators then orchestrate the inflammatory response, eliciting its various vascular and cellular components. Dead cells also release danger signals that activate dendritic cells and promote the generation of immune responses to antigens. Here we review what is presently known about the sterile inflammatory response and its underlying mechanisms.
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