Chemokine (C-C Motif) Receptor 3 Proteins (CCR3)

Human Chemokine (C-C Motif) Receptor 3 (CCR3) interaction partners

1. Sequential activation of CCR3 and then PGD2 receptors by autocrine ligands in response to leptin stimulation of eosinophils culminates with eosinophil activation, characterized by assembly of lipidic cytoplasmic platforms synthesis and secretion of the pleiotropic lipid mediators, PGD2, and LTC4. Study results suggested involvement of H-PGDS, rather than L-PGDS, in leptin-induced synthesis of PGD2 by eosinophils.

2. MACs from Familial hypercholesterolemia (FH)-MACs have an inflammatory phenotype that is characterized by the up-regulation of CCR3, CCR4, and CXCR1 under the control of miR-505-3p. These results suggest a chronic inflammatory condition in FH innate immunity cells that is not reverted by standard lipid-lowering treatment

3. CCR3 exists as a mixture of monomers and dimers under nearly physiological conditions. The monomeric CCR3 receptor is the minimal functional unit in cellular signal transduction. Agonists increase dimers and oligomers at high concentrations. Antagonists do not affect oligomeric status. Monomeric CCR3 exhibits a stronger chemotactic response in the migration assay of stably transfected CCR3 cells.

4. Study shows that CCR3, receptor of CCL28, was highly expressed in vascular endothelial cells in lung adenocarcinoma and is targeted by CCL28 to regulate angiogenesis.

5. Findings suggest that CCL11-CCR3 binding is involved in the progression of GBM.

6. Data show that high mRNA expression of CCR3 was related with improved relapse-free survival in luminal-A/B.

7. the expression of CCR3 on dispersed synovial tissue and peripheral blood cells in rheumatoid arthritis, was investigated.

8. Chemokine receptors CCR3 and CCR4, and the mucosa specific chemokine CCL28 have predominant roles in oral wound healing by increasing human gingiva fibroblast proliferation, migration, and the secretion of IL-6 and HGF and reducing the secretion of TIMP-1.

9. simvastatin was demonstrated to inhibit IL-5-induced CCR3 expression and chemotaxis of eosinophils mediated via the mevalonate pathway.

10. Data indicate that approximately 4.5% dispersed osteoarthritis (OA) synovial tissue cells are CC chemokine receptor CCR 3 (CCR3)+ cells.

11. This meta-analysis provides robust estimates that interleukin 18 receptor accessory protein rs917997 and chemokine (C-C motif) receptor 3 rs6441961 are potential risk factors for celiac disease in European populations.

12. Results highlight the potential role of CCR genes in narcolepsy and support the hypothesis that patients with narcolepsy have impaired immune function.

13. Periprostatic adipocytes drive prostate cancer progression in obesity via CCL7 secretion which stimulates CCR3 expressing tumor cells.

14. Results show the structure of CCL11 bound to the sulfated N-terminal region of its receptor CCR3 and show that intact CCR3 is sulfated and sulfation enhances receptor activity.

15. CCL28-CCR3 interactions are involved in the homeostatic trafficking of CD4(+) T cells to the upper airways.

16. In vitro chemotaxis assay indicates dominant role of RANTES and IP-10 in the selective recruitment of CXCR3(+)CCR5(+)cells at the tubercular pathologic sites.

17. CCR3-driven communication pathways from the epidermis to the dermis may modulate tissue remodeling in atopic skin inflammation.

18. Increased expression of CCR1 and CCR3 chemokine receptors may, in accord with various chemokines, contribute to the pathogenesis of nasal polyposis.

19. Retinoic acids up-regulate functional eosinophil-driving receptor CCR3.

20. CCR3 demonstrates adequate sensitivity (83%) but weak specificity (59%) in its ability to reliably identify histamine-releasing activated basophils.

Mouse (Murine) Chemokine (C-C Motif) Receptor 3 (CCR3) interaction partners

1. CD193(+) neutrophils increase in number under inflammatory conditions due to chronic IL-21 production.

2. CCR3 gene knockout may alleviate Eosinophil (EOS) invasion and the inflammatory response in allergic rhinitis model mice by reducing the expression levels of EOS peroxidase, EOS cationic protein, major basic protein, IL4, and IgE, and increasing the expression of IL10 and IFNgamma.

3. We found abnormalities in sleep patterns in the resting phase and in the number of Hcrt neurons in Ccr3 KO mice. These observations suggest a role for CCR3 in sleep-wake regulation in narcolepsy patients

4. Study found that CCR3 plays a crucial role in neuronal injury. CCR3 deletion or inhibition protects neurons from oxygen-glucose-deprivation-induced cytotoxicity in primary cortical cultures. CCR3 KO mice also displayed significant reduction of infarct volume in the brain after experimental stroke.

5. Retinal inhibition of CCR3 induces retinal cell death in a murine model of choroidal neovascularization.

6. Periprostatic adipocytes drive prostate cancer progression in obesity via CCL7 secretion which stimulates CCR3 expressing tumor cells.

7. The RNA interference therapy to CCR3 by local administration pernasal can suppress the process of the development, migration and invasion of the allergic rhinitis eosinophil.

8. Chemokine CCR3 ligands-binding peptides derived from a random phage-epitope library.

9. CCR3 plays no role in choroidal neovascularization development.

10. The collective data suggest that activation of the CB2R results in "cross-talk" with CCR-3, resulting in decreased migratory responsiveness to Tat.

11. CCR3 plays no significant role in choroidal neovascularization development.

12. The CCR3/eotaxin pathway is involved in the regulation of allergen-driven in situ haematopoiesis and the accumulation/mobilization of eosinophil-lineage-committed progenitor cells in the lung.

13. Trafficking to the cell surface of nascent CCR3 is critically dependent on a C-terminal leucine residue, suggestive of specific mechanisms for CCR3 export.

14. CCR3-deficiency does not alter mast cell phenotype or ability to migrate in vitro

15. CCR3 is essential for skin eosinophilia and airway hyperresponsiveness in a murine model of allergic skin inflammation.

16. 3-fold increased expression in IL-5 transgenic mice leads to increased responsiveness of eosinophils to eotaxin

17. role of CCR3 in the endogenous mechanisms involved in the inflammatory cell recruitment in an experimental model of allergic cutaneous reaction

18. CCR3 is constitutively expressed on CD34+ progenitor cells obtained from cord blood, and it behaves as a functional receptor as it transduces in vitro and in vivo chemotactic responses after binding to its ligand eotaxin.

19. Eosinophils survive longer under the influence of CCR3-reactive chemokines, which aid the infiltration of these cells into the tissue and that eosinophils may survive even longer if they encounter survival factors at local inflammatory sites.

20. Distinct acidic and basic residues within CCR3 determine both receptor expression and activation by the eotaxins.

Guinea Pig Chemokine (C-C Motif) Receptor 3 (CCR3) interaction partners

1. The expression of CCR3 in the bone marrow and peripheral tissue with allergic asthma was significantly higher than that in the controls.