Pathogenicity of autoreactive TH17 cells is modulated by the TRPM7 kinase

Elevated TRPM7 activity in CSF-derived T effector cells from multiple sclerosis patients is linked to higher TRPM7 expression on human TH17 cells, implicating TRPM7 in pathogenic TH17 biology.

• Why it matters: Pathogenic TH17 cells drive autoimmune disease, but how TRPM7 kinase activity shapes their polarization, migration, and reactivation in MS remains unclear.
• What they did: Using human T cells and murine experimental autoimmune encephalomyelitis, the study compared MS CSF T effector cells and TH17 TRPM7 expression, then tested Trpm7R/R mice with disrupted kinase activity versus Trpm7+/+ controls.
• The result: Trpm7R/R mice showed impaired pathogenic TH17 differentiation and a significantly milder TH17-mediated transfer EAE course, with increased CNS FOXP3+ T cells but reduced TH17 CNS infiltration due to migration and intestinal reactivation defects.

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