Cell therapy regimens are frequently compromised by low-efficiency cell homing to therapeutic niches. Improvements in this regard would enhance effectiveness of clinically applicable cell therapy. The major regulators of tissue-specific cellular migration are chemokines, and therefore selection of therapeutic cellular populations for appropriate chemokine receptor expression would enhance tissue-homing competence.
View Article and Find Full Text PDFChemokines direct leukocyte migration by activating intracellular signalling pathways through G-protein coupled chemokine receptors. However, they also bind to other surface proteins, including a group of molecules which we refer to as 'atypical' chemokine receptors. One such molecule is D6.
View Article and Find Full Text PDFD6 is a heptahelical receptor that suppresses inflammation and tumorigenesis by scavenging extracellular pro-inflammatory CC chemokines. Previous studies suggested this is dependent on constitutive trafficking of stable D6 protein to and from the cell surface via recycling endosomes. By internalizing chemokine each time it transits the cell surface, D6 can, over time, remove large quantities of these inflammatory mediators.
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