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Although the molecular mechanisms regulating HIV chemokine receptors in the cervix are unclear, inflammatory prostaglandins derived by metabolism of arachidonic acid by cyclo-oxygenase enzymes (COX-1 and COX-2)[9] have been shown to regulate HIV chemokine expression in uterine epithelial cells in the female genital tract.
3] Nonstandard abbreviations: CSC, cancer stem cell; SDF-1, stromal-derived factor 1; CXCR4, C-X-C chemokine receptor type 4.
Ransohoff and his colleague Robert Miller, PhD (Case Western University), showed that deactivating a specific chemokine receptor enhanced the development of the myelin-producing cells in rodents, and allowed for damaged myelin to be repaired (The Journal of Neuroscience 1998;18:10457-10463).
CCX354 has been shown to be a potent and selective antagonist of CCR1, a chemokine receptor that drives the recruitment of certain inflammatory cells including populations of monocytes, macrophages and T cells into the joints of patients with RA.
Ligands (RANTES, MIP-1[alpha], MIP1[beta]) of this chemokine receptor were also secreted in lesser quantity from MO/Mo of HNSCC patients, in comparison to healthy individuals.
In studies looking at chemokine receptor expression and function in osteosarcoma cell lines and tissues from osteosarcoma patients, the results showed that messenger RNA (mRNA) and protein expression of CXCR4 were correlated with neoplastic progression, in line with other solid tumors.
Resistance to HIV-1 infection in Caucasian individuals bearing mutant alleles of the CCR-5 chemokine receptor gene.
Specifically, how C-X-C chemokine receptor type 4 (CXCR4), C-X-C chemokine receptor type 7 (CXCR7), C-X-C chemokine ligand 12 (CXCR12), and doublecortin (DCX) affect migration of neural pathways in relation to VEGF.
CC chemokine receptor 5 (CCR5) is involved in the chemotaxis of leukocytes towards inflammatory sites (Baggiolini, 1998), and is present only in certain cell types, such as lymphocytes, dendritic cells and macrophages (Loetscher et al.
Some years ago we started evaluating the effect of highly active anti-retroviral therapy (HAART) at the level of CC chemokine production and chemokine receptor expression in a selected population of HIV-1 infected individuals showing a moderate immunodeficiency and mostly naive for antiretroviral therapy (19-22).
Macrophage-tropic (M-tropic) strains infect primary macrophages and primary lymphocytes and use the chemokine receptor CCR5 as a co-receptor.
Virus isolates recovered from infected individuals in the early stages of disease utilize chemokine receptor CCR5 (R5) exclusively as a coreceptor for cellular infection and do not induce syncitium formation in transformed T-cell lines in vitro (non-syncitium inducing or NSI).