4.7 Editorial Material

Kissing genetic MS risk loci to life

期刊

EBIOMEDICINE
卷 72, 期 -, 页码 -

出版社

ELSEVIER
DOI: 10.1016/j.ebiom.2021.103594

关键词

Multiple sclerosis; EBV

资金

  1. Cancer Research Switzerland [KFS-4962-02-2020]
  2. Cancer Research Center Zurich
  3. Sobek Foundation
  4. Swiss Vaccine Research Institute
  5. Roche
  6. Swiss National Science Foundation [310030B_182827, 310030L_197952/1, CRSII5_180323]
  7. Innosuisse
  8. Novartis
  9. KFSP-PrecisionMS of the University of Zurich
  10. HMZ ImmunoTargET of the University of Zurich
  11. Swiss National Science Foundation (SNF) [310030L_197952] Funding Source: Swiss National Science Foundation (SNF)

向作者/读者索取更多资源

Multiple sclerosis is an inflammatory autoimmune demyelinating disease that predominantly affects young adults, especially women, with genetic and environmental factors playing a role in its development. The major histocompatibility complex II gene locus and altered immune responses to the Epstein Barr virus are significant risk factors for the disease.
Multiple sclerosis (MS) is an inflammatory autoimmune demyelinating disease of the central nervous system (CNS) [1]. Its debilitating effects on sensory, motor, autonomic, and neurocognitive functions affect primarily young adults, especially women (two to three times more frequent than in men), and is most frequent in northern countries, affecting more than 150 individuals of every 100,000 inhabitants e.g. in Canada and the Scandinavian countries. The development of this often initially relapsing/remitting and later progressive dis-ease is associated with genetic and environmental risk factors [1, 3]. The major histocompatibility complex (MHC) class II gene locus is by far the most prominent genetic risk factor, and altered immune responses to the Epstein Barr virus (EBV), the causative infectious agent of most cases of infectious mononucleosis or kissing disease, have in recent years emerged as the most prominent environment induced risk factors for MS [1]. Interestingly, particularly infectious mononucleosis as symptomatic primary EBV infection, caused by a lymphocytosis of mainly lytic EBV antigen specific CD8+ T cells, and elevated antibody responses against EBV have been found to synergize with the MS associated MHC class II molecule HLA-DRB1*1501 to increase MS risk seven-to fifteen-fold, respectively [1]. Moreover, EBV infection seems to precede MS onset by several years in nearly all patients. Thus, EBV infection currently appears as a prerequisite for MS development that increases the risk for this autoimmune disease in genetically susceptible individuals. (C) 2021 The Author(s). Published by Elsevier B.V.

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