Introduction of CCR-3
CCR-3, alternatively known as eosinophil eotaxin receptor or CD antigen (CD193), belongs to family 1 of the G protein-coupled receptors for C-C type chemokines and it is encoded by CCR3 gene in human. CCR-3 can bind and respond to a range of chemokines, such as CCL5 (RANTES), CCL7 (MCP-3), CCL11 (eotaxin), CCL13 (MCP-4), and CCL26 (eotaxin-3). This receptor is highly expressed in basophils and eosinophils, and it can also be found in TH1 and TH2 cells, as well as in airway epithelial cells. The transcript variants by alternatively spliced have been described.
|Basic Information of CCR-3|
|Protein Name||C-C chemokine receptor type 3|
|Aliases||Eosinophil eotaxin receptor, CD193, CC-CKR-3, CKR3|
|Organism||Homo sapiens (Human)|
Function of CCR-3 Membrane Protein
Eotaxin has been proved to be a predominant ligand for the seven-transmembrane G protein-coupled receptor CCR-3. CCR-3 is highly expressed on primary human eosinophils, which is consistent with the potential ability of eotaxin to selectively influence the migration of these cells. When binding with its ligands, CCR-3 transduces a signal by increasing the intracellular calcium ions level. CCR-3 may play a crucial role in the accumulation and activation of eosinophils, which is a leukocyte population involved in many inflammatory pathologies including asthma, as well as other inflammatory cells in the allergic airway. It is also supposed to be an alternative coreceptor with CD4 for HIV-1 infection. Also, overexpression of CCR-3 together with its ligands seems to be a characteristic of ulcerative colitis (UC). The production of CCR-3 ligands by human colonic epithelial cells further indicate that the epithelium is responsible for modulating pathological T-cell-mediated mucosal inflammation. A study of CCR-3 antagonist has indicated that it can remarkably reduce eosinophil infiltration of the airways followed by a normalization of airway hyperresponsiveness, reduced mucus production, and prevention of airway remodeling.
Application of CCR-3 Membrane Protein in Literature
1. Milica G., et al. Novel Peptide Nanoparticle Biased Antagonist of CCR3 Blocks Eosinophil Recruitment and Airway Hyperresponsiveness. Journal of Allergy and Clinical Immunology. 2018. PubMed ID: 29778505
This article reports that R321 is a potent and selective antagonist of the CCR3 signaling cascade. Inhibition through a biased mode of antagonism may hold significant therapeutic promise by eluding the formation of drug tolerance.
2. Chang X., et al. Upregulated expression of CCR3 in osteoarthritis and CCR3 mediated activation of fibroblast-like synoviocytes. Cytokine. 2016, 77: 211-9. PubMed ID: 26409848
This article reveals that FLS via eotaxin-1 and its receptor CCR3 plays an important role in the pathogenesis of OA, which strengthen the concept that OA is likely an inflammation-related disease.
3. Danilova E., et al. A role for CCL28-CCR3 in T-cell homing to the human upper airway mucosa. Mucosal Immunol. 2015, 8(1): 107-14. PubMed ID: 24917456
The outcome of this study indicates that CCL28-CCR3 interactions are involved in the homeostatic trafficking of CD4+ T cells to the upper airways.
4. Neighbour H., et al. Safety and efficacy of an oral CCR3 antagonist in patients with asthma and eosinophilic bronchitis: a randomized, placebo-controlled clinical trial. Clin Exp Allergy. 2014, 44(4): 508-16. PubMed ID: 24286456
This study calls into question the role of CCR3 in airway eosinophilia in asthma and suggests that other cellular mechanisms mediated by the CCR3 receptor may contribute to airway hyperresponsiveness.
5. Dosanjh A. Activation of eosinophil CCR3 signaling and eotaxin using a bioinformatics analysis of a mouse model of obliterative airway disease. Mol Metab. 2014, 34(7): 543-6. PubMed ID: 24702154
This article suggests that the eosinophil signaling pathway CCR3 and eotaxin were significantly expressed in chronic allograft rejection, and also imply a role in controlling early alloimmune damage in controls.
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