AI Article Synopsis
- Leukocyte migration into the central nervous system is a key factor in the development of multiple sclerosis, but the specific mechanisms controlling this migration are still unclear.
- Researchers found that a protein called junctional adhesion molecule-like is significantly increased in the blood-brain barrier and among certain immune cells in multiple sclerosis patients.
- Blocking this protein reduced the ability of immune cells to migrate, suggesting that junctional adhesion molecule-like could be a potential target for new treatments.
Article Abstract
Leukocyte transmigration into the central nervous system promotes multiple sclerosis pathogenesis, yet ambiguity remains regarding the mechanisms controlling the migration of distinct immune cell subsets. Using in vitro, ex vivo and postmortem human materials, we identified a significant upregulation of junctional adhesion molecule-like expression at the blood-brain barrier, monocytes, and CD8 T cells of multiple sclerosis patients. We also detected junctional adhesion molecule-like(+) trans-migratory cups when monocytes/CD8 T cells adhered to the blood-brain barrier, however, their migratory capacity was significantly compromised when junctional adhesion molecule-like was blocked. These findings highlight a novel role for junctional adhesion molecule-like in leukocyte transmigration and its potential as a promising therapeutic target.
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Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4693623 | PMC |
| http://dx.doi.org/10.1002/acn3.255 | DOI Listing |
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