CCR6-CCL20 axis as a therapeutic target for autoimmune diseases
Autoimmunity Reviews, ISSN: 1568-9972, Vol: 20, Issue: 7, Page: 102846
2021
- 111Citations
- 63Captures
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Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
Citation Benchmarking is provided by Scopus and SciVal and is different from the metrics context provided by PlumX Metrics.
Metrics Details
- Citations111
- Citation Indexes111
- 111
- CrossRef42
- Captures63
- Readers63
- 63
Review Description
Chemokine receptor CCR6 is expressed on various cells such as B cells, immature dendritic cells, innate lymphoid cells (ILCs), regulatory CD4 T cells, and Th17 cells. CCL20 is the only known high-affinity ligand that binds to CCR6 and drives CCR6 + cells' migration in tissues. CCL20 is mainly produced by epithelial cells, and its expression is increased by several folds under inflammatory conditions. Genome-wide association studies (GWAS) in patients with inflammatory bowel disease (IBD), psoriasis (PS), rheumatoid arthritis (RA), and multiple sclerosis (MS) showed a very strong correlation between the expression of CCR6 and disease severity. It has been shown that disruption of CCR6-CCL20 interaction by using antibodies or antagonists prevents the migration of CCR6 expressing immune cells at the site of inflammation and reduces the severity of the disease. This review discussed the importance of the CCR6-CCL20 axis in IBD, PS, RA, and MS, and recent advances in targeting the CCR6-CCL20 in controlling these autoimmune diseases.
Bibliographic Details
http://www.sciencedirect.com/science/article/pii/S156899722100118X; http://dx.doi.org/10.1016/j.autrev.2021.102846; http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=85105552128&origin=inward; http://www.ncbi.nlm.nih.gov/pubmed/33971346; https://linkinghub.elsevier.com/retrieve/pii/S156899722100118X; https://dx.doi.org/10.1016/j.autrev.2021.102846
Elsevier BV
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