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Review
. 2014 Jun;155(6):961-73.
doi: 10.1016/j.surg.2014.02.006. Epub 2014 Feb 8.

Chemokines and chemokine receptors: update on utility and challenges for the clinician

Ishan Roy  1 , Douglas B Evans  2 , Michael B Dwinell  3
Affiliations
Review

Chemokines and chemokine receptors: update on utility and challenges for the clinician

Ishan Roy et al. Surgery. 2014 Jun.
No abstract available

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Figures

Fig
Fig
Schematic overview of chemokine function in intestinal epithelium. Pathologically established gradients of chemokine proteins lead to aberrant migration of cells in multiple ways. Herein, we describe the differing roles of chemokines by using the intestinal epithelium as a model tissue site of dysregulated chemokine production. (A) Acute or chronic inflammation resulting from epithelial barrier disruption, pathogen infection, or other stimuli, leads to increased chemokine secretion. As a result, new local chemokine gradients attract immune cells from the circulatory system into to the site of inflammation. (B) A contrasting gradient is seen during human cancer malignancy, specifically in the CXCL12-CXCR4 axis. Dysplastic lesions contain heterogeneous groups of cells, including some that lose expression of homeostatically produced chemokines, such as CXCL12. Within malignant tumors, those cells that lack CXCL12 ligand expression and retain CXCR4 receptor expression are able to migrate toward existing local gradients of chemokine expression. Primary sources of CXCL12 gradients include neighboring fibroblasts and endothelial cells. Thus, cancer cells lacking ligand expression are capable of following a new gradient into circulation. (C) Those cancer cells that lack CXCL12 ligand expression and survive in circulation can then migrate to distant organs with constitutively high CXCL12 expression, such as the liver, lung, or bone. Within the vessels of these distant sites, cancer cells then follow a new chemokine gradient established by both the endothelial and parenchymal cells, engendering metastases.
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