Example sentences for: cxc
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The CXC chemokines such as IL-8 were originally identified as potent activators and chemoattractants for neutrophils, whereas the CC chemokines such as MCP-1 and RANTES mostly attract monocytes and eosinophils respectively [ 10 ] . Chemokines are secreted in a stimulus-and cell type-specific manner [ 11 12 13 14 15 16 17 ] and are regulated primarily at the level of gene transcription [ 18 19 20 21 22 23 24 ] . The transcriptional promoters of IL-8, RANTES and MCP-1 contain binding sites for the redox-responsive transcription factor NF-κB, which has been shown to be important for their regulation by viral infections and cytokines [ 18 20 23 25 26 27 28 29 30 31 32 33 34 ] .
The first evidence that chemokines are associated with wound healing in vivo was reported in 1990 using the chemokine cCAF (chicken Chemotactic and Angiogenic Factor; the product of the 9E3 gene), a CXC chemokine that is now known to be the ortologue for human IL-8 [ 9 ] . cCAF is expressed to high levels very shortly after wounding and during the first 24-48 hours after injury, and remains elevated for at least 16 days after wounding [ 6 10 ] . It is primarily expressed by the fibroblasts of the granulation tissue, especially where interstitial collagen (Coll) is abundant, but the levels are also high in the endothelial cells of the microvessels, in the healing epidermis and in the connective tissue beneath the skin [ 6 11 ] . In the chicken chorioallantoic membrane (CAM) assay, low concentration of cCAF results in chemotaxis of monocyte/macrophages and lymphocytes and the formation of a granulation-like tissue beneath the chemokine-containing pellet [ 3 ] . After four days of exposure to this chemokine, the ectoderm of the CAMs becomes thickened and the amount of fibrillar collagen in the tissue is markedly increased, strongly suggesting that cCAF is able to initiate some of the primary events that lead to granulation tissue formation [ 3 ] .
ELR +CXC chemokines are potent angiogenic factors, whereas ELR -CXC chemokines are potent angiostatic factors.
Sepsis is associated with a rapid release of CXC chemokines by alveolar macrophages, as well as up regulation of lung vascular intercellular adhesion molecule-1 (ICAM-1) expression [ 26 ] and these may contribute to the initial increase in adherent vascular neutrophils in the lung.
MIG/CXCL 9 and IP-10/CXCL10 are glutamine-leucine-arginine (ELR)-negative CXC chemokines that are potent chemoattractants for activated T cells [ 11 12 13 ] . These chemokines also have in common the ability to signal through a G protein-coupled receptor, CXCR3, expressed on activated T lymphocytes.
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