TAM receptor signaling dictates lesion location and clinical phenotype during experimental autoimmune encephalomyelitis-Reference-Cited by-同舟云学术

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TAM receptor signaling dictates lesion location and clinical phenotype during experimental autoimmune encephalomyelitis

Published:2023-02 Issue: Volume:375 Page:578016
ISSN:0165-5728
Container-title:Journal of Neuroimmunology
language:en
Short-container-title:Journal of Neuroimmunology

Author:

Gardner Ashley Munie,Atkinson Jeffrey R.,Wilkinson Nicole M.,Jerome Andrew D.,Bellinger Calli E.,Sas Andrew R.,Segal Benjamin M.

Funder

Foundation for the National Institutes of Health

National Institutes of Health

Publisher

Elsevier BV

Subject

Neurology (clinical),Neurology,Immunology,Immunology and Allergy

Reference40 articles.

1. Infiltrating monocytes trigger EAE progression, but do not contribute to the resident microglia pool;Ajami;Nat. Neurosci.,2011

2. Common and low frequency variants in MERTK are independently associated with multiple sclerosis susceptibility with discordant association dependent upon HLA-DRB1*15:01 status;Binder;PLoS Genet.,2016

3. Differential induction of interleukin-1beta and tumour necrosis factor-alpha may account for specific patterns of leukocyte recruitment in the brain;Blond;Brain Res.,2002

4. T-helper cell diversity in experimental autoimmune encephalomyelitis and multiple sclerosis;Carbajal;J. Immunol.,2015

5. Anti-Axl antibody treatment reduces the severity of experimental autoimmune encephalomyelitis;DuBois;J. Neuroinflammation,2020

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