Defective fractalkine-CX3CR1 signaling aggravates neuroinflammation and affects recovery from cuprizone-induced demyelination.

ABSTRACT: Microglia have been implicated in multiple sclerosis (MS) pathogenesis. The fractalkine receptor CX3CR1 limits the activation of pathogenic microglia and the human polymorphic CX3CR1^I249/M280 (hCX3CR1^I249/M280 ) variant increases disease progression in models of MS. However, the role of hCX3CR1^I249/M280 variant on microglial activation and central nervous system repair mechanisms remains unknown. Therefore, using transgenic mice expressing the hCX3CR1^I249/M280 variant, we aimed to determine the contribution of defective CX3CR1 signaling to neuroinflammation and remyelination in the cuprizone model of focal demyelination. Here, we report that mice expressing hCX3CR1^I249/M280 exhibit marked demyelination and microgliosis following acute

SUBMITTER: Mendiola AS 

PROVIDER: S-EPMC9427683 | biostudies-literature | 2022 Sep

REPOSITORIES: biostudies-literature