Myeloid Kruppel-like factor 2 deficiency exacerbates neurological dysfunction and neuroinflammation in a murine model of multiple sclerosis.

Abstract

Cells of the innate immune system are important mediators of multiple sclerosis (MS). We have previously identified Kruppel-like factor 2 (KLF2) as a critical negative regulator of myeloid activation in the setting of bacterial infection and sepsis, but the role of myeloid KLF2 in MS has not been investigated. In this study, myeloid KLF2 deficient mice exhibited more severe neurological dysfunction and increased spinal cord demyelination and neuroinflammation in experimental autoimmune encephalomyelitis. This study represents the first description of a significant role of myeloid KLF2 in neuroinflammation, identifying KLF2 as a potential target for further investigation in patients with MS.