Defective sphingosine 1-phosphate receptor 1 (S1P1) phosphorylation exacerbates TH17-mediated autoimmune neuroinflammation

被引：0
|
作者：
Christopher S Garris
Linfeng Wu
Swati Acharya
Ahmet Arac
Victoria A Blaho
Yingxiang Huang
Byoung San Moon
Robert C Axtell
Peggy P Ho
Gary K Steinberg
David B Lewis
Raymond A Sobel
David K Han
Lawrence Steinman
Michael P Snyder
Timothy Hla
May H Han
机构：
[1] Stanford University School of Medicine,Department of Neurology and Neurological Sciences
[2] Graduate Program in Immunology,Division of Medical Sciences
[3] Harvard Medical School,Department of Genetics
[4] Stanford University School of Medicine,Department of Pediatrics, Division of Allergy
[5] Immunology and Rheumatology,Department of Neurosurgery
[6] Stanford University School of Medicine,Department of Pathology and Laboratory Medicine
[7] Center for Vascular Biology,Department of Pathology
[8] Weill Cornell Medical College,Department of Cell Biology
[9] Cornell University,undefined
[10] Stanford University School of Medicine,undefined
[11] Center for Vascular Biology,undefined
[12] University of Connecticut Health Center,undefined
来源：
Nature Immunology | 2013年 / 14卷
关键词：
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学科分类号：
摘要：
S1P1 is a sphingosine phosphate receptor expressed on lymphocytes. Han and colleagues show that phosphorylated S1P1 accumulates in brain lesions of patients with multiple sclerosis. Similarly, mice bearing mutant S1P1 develop more severe experimental autoimmune encephalomyelitis.
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页码：1166 / 1172
页数：6
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