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Updated: Jul 15, 2026
Induction and Clinical Scoring of Chronic-Relapsing Experimental Autoimmune Encephalomyelitis
Published on: July 4, 2007
TAM receptor signaling dictates lesion location and clinical phenotype during experimental autoimmune
Ashley Munie Gardner1, Jeffrey R Atkinson2, Nicole M Wilkinson3
1Department of Neurology, The Ohio State University, 395 W. 12th Ave., 7th Floor, Columbus, OH 43210, USA; The Neuroscience Research Institute, The Ohio State University, 395 W. 12th Ave., 7th Floor, Columbus, OH 43210, USA; Graduate Program in Immunology, University of Michigan Medical School, 2978 Taubman Health Sciences Library, 1135 Catherine, Ann Arbor, MI 48109, USA.
Abstract:
Experimental autoimmune encephalomyelitis (EAE), induced by the adoptive transfer of Th17 cells, typically presents with ascending paralysis and inflammatory demyelination of the spinal cord. Brain white matter is relatively spared. Here we show that treatment of Th17 transfer recipients with a highly selective inhibitor to the TAM family of tyrosine kinase receptors results in ataxia associated with a shift of the inflammatory infiltrate to the hindbrain parenchyma. During homeostasis and preclinical EAE, hindbrain microglia express high levels of the TAM receptor Mer. Our data suggest that constitutive TAM receptor signaling in hindbrain microglia confers region-specific protection against Th17 mediated EAE.
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