Objective: c-Met, a tyrosine kinase receptor, is the unique receptor for hepatocyte growth factor (HGF). The HGF/c-Met axis is reported to modulate cell migration, maturation, cytokine production, and antigen presentation. Here, we report that CD4c-Met T cells are detected at increased levels in experimental autoimmune encephalomyelitis (EAE), a mouse model of multiple sclerosis (MS).
Methods: c-Met expression by CD4 T cells was analyzed mostly by flow cytometry and by immunohistochemistry from mice and human PBMCs. The in vivo role of CD4c-Met T cells was assessed in EAE.
Results: CD4c-Met T cells found in the CNS during EAE peak disease are characterized by a pro-inflammatory phenotype skewed towards a Th1 and Th17 polarization, with enhanced adhesion and transmigration capacities correlating with increased expression of integrin α4 (Itgα4). The adoptive transfer of Itgα4-expressing CD4Vα3.2c-Met T cells induces increased disease severity compared to CD4Vα3.2c-Met T cells. Finally, CD4c-Met T cells are detected in the brain of MS patients, as well as in the blood with a higher level of Itgα4. These results highlight c-Met as an immune marker of highly pathogenic pro-inflammatory and pro-migratory CD4 T lymphocytes associated with neuroinflammation.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC9052663 | PMC |
| http://dx.doi.org/10.1186/s12974-022-02461-7 | DOI Listing |
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