The DOI matches its Crossref record; 145 of the 145 references it cites were found in a registry or an index.
Molecular mechanisms of innate memory and tolerance to LPS
Abstract
LPS is a potent trigger of macrophage-mediated inflammation. However, prolonged exposure to LPS induces a state of tolerance that reprograms the inflammatory response, resulting in reduced inflammatory cytokine production in vitro and in vivo. Recent evidence suggests that LPS tolerance also increases the expression of a subset of genes that may protect animals from systemic infection while they are in the tolerized state. However, a molecular basis for these selective changes in inflammatory gene expression during LPS tolerance has remained elusive. In this review, we discuss the molecular mechanisms that may account for these effects, focusing on changes in LPS signaling, epigenetic markers, and chromatin remodeling that may be responsible for cellular memory and physiologic changes that comprise the LPS tolerance phenomenon.
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Metadata
- Authors
- Seeley, J. J., & Ghosh, S.
- Venue
- Journal of Leukocyte Biology
- Publisher
- Oxford University Press (OUP)
- Published
- 2016-10-25
- Volume
- 101
- Issue
- 1
- Pages
- 107-119
- ISSN
- 0741-5400 (ISSN-L)
- 1938-3673
- OpenAlex
- W2545733225
- Cited by
- 367
- References
- 145
- FWCI
- 9.76
- Type
- journal article
- Language
- en
- Open access
- closed
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.
