Table 1.

Summary of the current in vivo studies supporting a role for the Gas6/TAM system in multiple sclerosis.

Author	Year	Main Findings
Hoehn et al. [97]	2008	The deletion of Axl is associated with a delayed recovery and prolonged axonal damage following cuprizone toxicity
Binder et al. [94]	2008	Gas6, Axl and MerTK are upregulated upon cuprizone-induced demyelination; Gas6 knockout (KO) mice have more severe demyelination
Weinger et al. [101]	2009	In chronic multiple sclerosis (MS) lesions sAxl and sMer are upregulated and inversely related to cerebrospinal fluid (CSF) Gas6 concentration
Tsiperson et al. [96]	2010	Gas6 stimulates remyelination following cuprizone toxicity
Ma et al. [104]	2011	SNPs in MerTK gene confer susceptibility to MS
Binder et al. [95]	2011	Gas6 KO mice show a defective remyelination, after cuprizone-induced demyelination, which can be corrected by administering exogenous Gas6
ANZgene consortium [103]	2011	Many SNPs of MerTK gene are associated to MS risk in a genome wide association study
Weinger et al. [100]	2011	Axl KO murine models of experimental allergic encephalomyelitis (EAE) are characterized by a more severe phenotype than wild type mice
Sainaghi et al. [110]	2013	Gas6 CSF concentration is higher in patients with shorter and less severe MS flares
Gruber et al. [99]	2014	Intracerebral delivery of Gas6 protects against damage in EAE
Hoppmann et al. [106]	2015	CD4+ T cells from EAE mice show an up-regulation of Gas6 and MerTK
Binder et al. [105]	2016	SNPs in MerTK can protect or confer risk of MS on the basis of HLA-DRB1*15:01