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CCL21/CCR7 axis as a therapeutic target for autoimmune diseases.

Authors :
Han, Le
Zhang, Lingling
Source :
International Immunopharmacology. Aug2023, Vol. 121, pN.PAG-N.PAG. 1p.
Publication Year :
2023

Abstract

[Display omitted] • Chemokine is key coordinator of leukocyte trafficking in inflammation immune response. • Inflammatory responses and immune regulation are crucial functions of CCL21/CCR7 axis. • CCL21 and CCR7 are highly expressed on various cells in autoimmune diseases. • Blocking CCL21-CCR7 signaling can alleviate autoimmune disease progression. • CCL21/CCR7 axis is a potential therapeutic target for autoimmune diseases. Chemokine receptor 7 (CCR7) is a G protein-coupled receptor containing 7 transmembrane domains that is expressed on various cells, such as naive T/B cells, central memory T cells, regulatory T cells, immature/mature dendritic cells (DCs), natural killer cells, and a minority of tumor cells. Chemokine ligand 21 (CCL21) is the known high-affinity ligand that binds to CCR7 and drives cell migration in tissues. CCL21 is mainly produced by stromal cells and lymphatic endothelial cells, and its expression is significantly increased under inflammatory conditions. Genome-wide association studies (GWAS) have shown a strong association between CCL21/CCR7 axis and disease severity in patients with rheumatoid arthritis, sjogren's syndrome, systemic lupus erythematosus, polymyositis, ankylosing spondylitis, and asthma. Disrupting CCL21/CCR7 interaction with antibodies or inhibitors prevents the migration of CCR7-expressing immune and non-immune cells at the site of inflammation and reduces disease severity. This review emphasizes the importance of the CCL21 /CCR7 axis in autoimmune diseases and evaluates its potential as a novel therapeutic target for these conditions. [ABSTRACT FROM AUTHOR]

Details

Language :
English
ISSN :
15675769
Volume :
121
Database :
Academic Search Index
Journal :
International Immunopharmacology
Publication Type :
Academic Journal
Accession number :
165123875
Full Text :
https://doi.org/10.1016/j.intimp.2023.110431