Eosinophil extracellular DNA traps: molecular mechanisms and potential roles in disease

Yousefi, Shida; Simon, Dagmar; Simon, Hans-Uwe (2012). Eosinophil extracellular DNA traps: molecular mechanisms and potential roles in disease. Current opinion in immunology, 24(6), pp. 736-9. Kidlington, UK: Elsevier 10.1016/j.coi.2012.08.010

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Eosinophil extracellular traps (EETs) are part of the innate immune response and are seen in multiple infectious, allergic, and autoimmune eosinophilic diseases. EETs are composed of a meshwork of DNA fibers and eosinophil granule proteins, such as major basic protein (MBP) and eosinophil cationic protein (ECP). Interestingly, the DNA within the EETs appears to have its origin in the mitochondria of eosinophils, which had released most their mitochondrial DNA, but were still viable, exhibiting no evidence of a reduced life span. Multiple eosinophil activation mechanisms are represented, whereby toll-like, cytokine, chemokine, and adhesion receptors can all initiate transmembrane signal transduction processes leading to the formation of EETs. One of the key signaling events required for DNA release is the activation of the NADPH oxidase. Here, we review recent progress made in the understanding the molecular mechanisms involved in DNA and granule protein release, discuss the presence of EETs in disease, speculate on their potential role(s) in pathogenesis, and compare available data on other DNA-releasing cells, particularly neutrophils.

Item Type:

Journal Article (Further Contribution)

Division/Institute:

04 Faculty of Medicine > Pre-clinic Human Medicine > Institute of Pharmacology
04 Faculty of Medicine > Department of Dermatology, Urology, Rheumatology, Nephrology, Osteoporosis (DURN) > Clinic of Dermatology

UniBE Contributor:

Yousefi, Shida; Simon, Dagmar and Simon, Hans-Uwe

ISSN:

0952-7915

Publisher:

Elsevier

Language:

English

Submitter:

Factscience Import

Date Deposited:

04 Oct 2013 14:35

Last Modified:

06 Dec 2013 13:36

Publisher DOI:

10.1016/j.coi.2012.08.010

PubMed ID:

22981682

Web of Science ID:

000312359600015

URI:

https://boris.unibe.ch/id/eprint/14102 (FactScience: 220911)

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