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- W1503617838 endingPage "480" @default.
- W1503617838 startingPage "471" @default.
- W1503617838 abstract "Traumatic brain injury (TBI) affects millions of people worldwide every year. The primary impact initiates the secretion of pro- and anti-inflammatory factors, subsequent recruitment of peripheral immune cells, and activation of brain-resident microglia and astrocytes. Chemokines are major mediators of peripheral blood cell recruitment to damaged tissue, including the TBI brain. Here we review the involvement of specific chemokine pathways in TBI pathology and attempts to modulate these pathways for therapeutic purposes. We focus on chemokine (C-C motif) ligand 2/chemokine (C-C motif) receptor 2 (CCL2/CCR2) and chemokine (C-X-C motif) ligand 12/chemokine (C-X-C motif) receptor 4 (CXCL12/CXCR4). Recent microarray and multiplex expression profiling have also implicated CXCL10 and CCL5 in TBI pathology. Chemokine (C-X3-C motif) ligand 1/chemokine (C-X3-C motif) receptor 1 (CX3CL1/CX3CR1) signaling in the context of TBI is also discussed. Current literature suggests that modulating chemokine signaling, especially CCL2/CCR2, may be beneficial in TBI treatment." @default.
- W1503617838 created "2016-06-24" @default.
- W1503617838 creator A5030147865 @default.
- W1503617838 creator A5034732141 @default.
- W1503617838 date "2015-07-01" @default.
- W1503617838 modified "2023-10-02" @default.
- W1503617838 title "Inflammatory reaction after traumatic brain injury: therapeutic potential of targeting cell–cell communication by chemokines" @default.
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- W1503617838 doi "https://doi.org/10.1016/j.tips.2015.04.003" @default.
- W1503617838 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/4485943" @default.
- W1503617838 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/25979813" @default.