The physiological roles of ICAM-1 and ICAM-2 in neutrophil migration into tissues

Lyck, Ruth; Enzmann, Gaby (2015). The physiological roles of ICAM-1 and ICAM-2 in neutrophil migration into tissues. Current opinion in hematology, 22(1), pp. 53-59. Wolters Kluwer Lippincott Williams & Wilkins 10.1097/MOH.0000000000000103

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PURPOSE OF REVIEW Neutrophil extravasation from the blood into tissues is initiated by tethering and rolling of neutrophils on endothelial cells, followed by neutrophil integrin activation and shear resistant arrest, crawling, diapedesis and breaching the endothelial basement membrane harbouring pericytes. Endothelial intercellular cell adhesion molecule (ICAM)-1 and ICAM-2, in conjunction with ICAM-1 on pericytes, critically contribute to each step. In addition, epithelial ICAM-1 is involved in neutrophil migration to peri-epithelial sites. The most recent findings on the role of ICAM-1 and ICAM-2 for neutrophil migration into tissues will be reviewed here. RECENT FINDINGS Signalling via endothelial ICAM-1 and ICAM-2 contributes to stiffness of the endothelial cells at sites of chronic inflammation and junctional maturation, respectively. Endothelial ICAM-2 contributes to neutrophil crawling and initiation of paracellular diapedesis, which then proceeds independent of ICAM-2. Substantial transcellular neutrophil diapedesis across the blood-brain barrier is strictly dependent on endothelial ICAM-1 and ICAM-2. Endothelial ICAM-1 or ICAM-2 is involved in neutrophil-mediated plasma leakage. ICAM-1 on pericytes assists the final step of neutrophil extravasation. Epithelial ICAM-1 rather indirectly promotes neutrophil migration to peri-epithelial sites. SUMMARY ICAM-1 and ICAM-2 are involved in each step of neutrophil extravasation, and have redundant but also distinct functions. Analysis of the role of endothelial ICAM-1 requires simultaneous consideration of ICAM-2.

Item Type:

Journal Article (Review Article)

Division/Institute:

04 Faculty of Medicine > Pre-clinic Human Medicine > Theodor Kocher Institute

UniBE Contributor:

Lyck, Ruth and Enzmann, Gaby

Subjects:

600 Technology > 610 Medicine & health

ISSN:

1065-6251

Publisher:

Wolters Kluwer Lippincott Williams & Wilkins

Language:

English

Submitter:

Ursula Zingg-Zünd

Date Deposited:

14 Mar 2016 15:02

Last Modified:

18 May 2016 18:34

Publisher DOI:

10.1097/MOH.0000000000000103

PubMed ID:

25427141

BORIS DOI:

10.7892/boris.77346

URI:

https://boris.unibe.ch/id/eprint/77346

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