Chemokine signaling in inflammation

Citation
Mp. Keane et Rm. Strieter, Chemokine signaling in inflammation, CRIT CARE M, 28(4), 2000, pp. N13-N26
Citations number
172
Categorie Soggetti
Aneshtesia & Intensive Care
Journal title
CRITICAL CARE MEDICINE
ISSN journal
00903493 → ACNP
Volume
28
Issue
4
Year of publication
2000
Supplement
S
Pages
N13 - N26
Database
ISI
SICI code
0090-3493(200004)28:4<N13:CSII>2.0.ZU;2-6
Abstract
The events that lead to an inflammatory response are characterized by recog nition of the site of injury by inflammatory cells, specific recruitment of subpopulations of leukocytes into tissue, removal of the offending agent a nd "debridement" of the injured cells/tissue, and repair of the site of inj ury with attempts to reestablish normal parenchymal, stromal, and extracell ular matrix relationship. The molecular regulation of this complex physiolo gic process involves the interaction between cell surface, extracellular ma trix, and soluble mediators, such as chemokines. Chemokine activities are m ediated through G-protein coupled receptors. This is the largest known fami ly of cell-surface receptors, which mediate transmission of stimuli as dive rse as hormones, peptides, glycopeptides, and chemokines. In this review, w e will focus on the signaling pathways involved in the production and funct ion of chemokines as they relate to the inflammatory response.