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proinflammatory factors, chemokines may also be produced in response to other tissue insults. Disruption of the cytoskeletal-nuclear architecture triggered by cellular stresses such as cell deformation, hypoxia, ischemia-reperfusion and particulate deposition activates the nuclear transcription factor NFkB to signal chemokine expression in the initiation, amplification and maintenance of inflammatory sequelae.

Chemokines and other chemotactic factors are recognized by specific cell surface receptors. Receptor numbers vary from a new hundred for TGF|3, which is chemotactically active at femtomolar concentrations, to nearly 100 000 for fMLP and C5a (C5aR, CD88), active in the nanomolar range. Two a chemokine receptors, which belong to a super-family of seven transmembrane G protein-coupled receptors, have been characterized on the surface of neutrophils: the type A receptor selectively binds IL-8, while the type B receptor binds all a chemokines which contain the sequence motif Glu-Leu-Arg (ELR) near the N-termini (IL-8, NAP2, GROa, (3, 7, and ENA-78) (Figure 3). The family of receptors for (3 chemokines is much more complex with at least five P chemokine receptors (CC CKR1-5) identified on mononuclear cells (monocytes, lymphocytes) and on basophils and eosinophils, each with varying specificities for different subsets of (3 chemokines. Interestingly, a chemokine receptor expressed on the surface of erythrocytes has broad specificity for both a and (3 chemokines, and may act as a scavenger receptor to remove chemokines from the circulation that might otherwise interfere with local chemotactic gradients. Occupancy of chemokine receptors, other than the erythrocyte chemokine receptor, transduces signals coupled to guanine nucleotide-binding (G) proteins which initiate a sequence of complex biochemical and cellular events. These events culminate in polarization of the cell wtih a redistribution of receptors and cytoskeletal elements (actin, myosin) towards the leading edge, extension of a lamellopod in the direction of the attractant (motile phenotype), and the initiation of directed movement toward the signal.

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