CXCR3 signaling reduces the severity of experimental autoimmune encephalomyelitis by controlling the parenchymal distribution of effector and regulatory T cells in the central nervous system.

@article{Mueller2007CXCR3SR,
  title={CXCR3 signaling reduces the severity of experimental autoimmune encephalomyelitis by controlling the parenchymal distribution of effector and regulatory T cells in the central nervous system.},
  author={Marcus Mueller and Sally L. Carter and Markus J Hofer and Peter M Manders and Daniel R. Getts and Meghan T. Getts and Angela Dreykluft and Bao Shi Lu and Craig Gerard and Nicholas J. C. King and Iain L Campbell},
  journal={Journal of immunology},
  year={2007},
  volume={179 5},
  pages={2774-86}
}
The chemokine receptor CXCR3 promotes the trafficking of activated T and NK cells in response to three ligands, CXCL9, CXCL10, and CXCL11. Although these chemokines are produced in the CNS in multiple sclerosis and experimental autoimmune encephalomyelitis (EAE), their role in the pathogenesis of CNS autoimmunity is unresolved. We examined the function of CXCR3 signaling in EAE using mice that were deficient for CXCR3 (CXCR3(-/-)). The time to onset and peak disease severity were similar for… CONTINUE READING

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