The Antimicrobial Peptide Cathelicidin Drives Development of Experimental Autoimmune Encephalomyelitis in Mice by Affecting Th17 Differentiation

It was released from neutrophils, microglia, and endothelial cells throughout disease; its interaction with T cells potentiates Th17 differentiation in lymph nodes and Th17 to exTh17 plasticity and IFN-γ production in the spinal cord.