CCR6-CCL20 axis as a therapeutic target for autoimmune diseases |
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| Authors: | Heikrujam Thoihen Meitei Nandadeep Jadhav Girdhari Lal |
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| Affiliation: | 1. Multiple Sclerosis Center, Department of Neurology, The Third Affiliated Hospital of Sun Yat-Sen University, Guangzhou, Guangdong Province, China;2. Department of Neurology, Guangdong 999 Brain Hospital, China;3. Centre for Neuromuscular and Neurological Disorders, University of Western Australia, Department of Neurology, Sir Charles Gairdner Hospital, Queen Elizabeth II Medical Centre, Perth, Australia;4. Institute of Immunology and Infectious Diseases, Murdoch University, Perth, Australia;1. Goldyne Savad Institute of Gene Therapy, Hebrew University Hospital, Jerusalem, Israel;2. Biokine Therapeutics Ltd, Ness Ziona, Israel;3. Neuroimmunology Laboratory, Department of Neurology, Tel Aviv Sourasky Medical Center, Tel Aviv, Israel;4. Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel;1. Department of Ophthalmology and Visual Science, Seoul St. Mary''s Hospital, College of Medicine, The Catholic University of Korea, Seoul, Korea;2. Catholic Institute of Visual Science, College of Medicine, The Catholic University of Korea, Seoul, Korea;3. Laboratory of Microbiology, College of Pharmacy, Ajou University, Suwon, Kyeonggi-do, Korea |
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| Abstract: | ![]()
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. |
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