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Cited by 287

The DOI matches its Crossref record; 141 of the 141 references it cites were found in a registry or an index.

Macrophages and Inflammatory Mediators in Chemical Toxicity: A Battle of Forces

Open access
Laskin, Debra L.·2009·Chemical Research in Toxicology
DOI 10.1021/tx900086v
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Abstract

Macrophages function as control switches of the immune system, providing a balance between pro- and anti-inflammatory responses. To accomplish this, they develop into different subsets: classically (M1) or alternatively (M2) activated macrophages. Whereas M1 macrophages display a cytotoxic, proinflammatory phenotype, much like the soldiers of The Dark Side of The Force in the Star Wars movies, M2 macrophages, like Jedi fighters, suppress immune and inflammatory responses and participate in wound repair and angiogenesis. Critical to the actions of these divergent or polarized macrophage subpopulations is the regulated release of inflammatory mediators. When properly controlled, M1 macrophages effectively destroy invading pathogens, tumor cells, and foreign materials. However, when M1 activation becomes excessive or uncontrolled, these cells can succumb to The Dark Side, releasing copious amounts of cytotoxic mediators that contribute to disease pathogenesis. The activity of M1 macrophages is countered by The Force of alternatively activated M2 macrophages, which release anti-inflammatory cytokines, growth factors, and mediators involved in extracellular matrix turnover and tissue repair. It is the balance in the production of mediators by these two macrophage subpopulations that ultimately determines the outcome of the tissue response to chemical toxicants.

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Metadata

Authors
Laskin, D. L.
Venue
Chemical Research in Toxicology
Publisher
American Chemical Society (ACS)
Published
2009-07-31
Volume
22
Issue
8
Pages
1376-1385
ISSN
  • 0893-228X (ISSN-L)
  • 1520-5010
DOI
10.1021/tx900086v
OpenAlex
W2053891616
Cited by
287
References
141
FWCI
6.49
Type
journal article
Language
en
Open access
green

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Bibliographic data: Semantic Scholar, OpenAlex, Crossref.

Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

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