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“Several lines of cancer cells (e.g., breast and prostate cancer cells), instead of normal epithelial cells, express a high level of CCR5, which help the cancer transformation process (Velasco-Velázquez et al., 2012; Daniela et al., 2014). Furthermore, the chemotherapy resistance of cancer stem cells could be partly accredited to the expression of CCR5 (Jiao et al., 2018).
In the CNS, these receptors are produced by microglia, astrocytes, and endothelial cells (normally undetectable on neurons) (Shukaliak and Dorovini-Zis, 2000; Mi et al., 2009; Subileau et al., 2009). All existing evidence suggests that CCR5 participates in neuroinflammation and neuroimmunology, including microglial activation (Cowell et al., 2006; Bokhari et al., 2009), microglial chemotaxis (Babcock Alicia et al., 2003; Kyung et al., 2010), monocyte/macrophage chemotaxis (Glass William and Lane Thomas, 2003), lymphocyte chemotaxis (Elodie et al., 2003; Glass William and Lane Thomas, 2003), brain development and cell differentiation (Bakhiet et al., 2001; Khan et al., 2003; Mi et al., 2009; Kyung et al., 2010), neuronal transmission (Adler et al., 2005; Chen et al., 2007; Veronica et al., 2008) and anti-microorganism functions (Mishra Saroj and Lothar, 2009; Haworth et al., 2017; Brelot and Chakrabarti, 2018). Under the same conditions, neuronal death was more notable in the brains of CCR5−/− mice than in those of CCR5+/+ mice (Hee et al., 2009). Knockout of the CCR5 gene was associated with the inadequate development and maturation of dopaminergic neurons (Choi et al., 2013).”