title: Serum levels of LIGHT in MS.
abstract: BACKGROUND
  Recently, a polymorphism in the LIGHT gene was shown to increase the risk of multiple sclerosis (MS) in a genome-wide association study (GWAS).
  
  
  OBJECTIVE
  Our aim was to investigate if serum levels of LIGHT were affected by this polymorphism and by the disease itself.
  
  
  METHODS
  Serum levels of LIGHT were investigated in four cohorts; 1) MS (n = 159) and controls (n = 160) in relation to rs1077667 genotype; 2) MS at relapse (n = 30) vs. healthy controls (n = 26); 3) MS (n = 27) vs. other neurological disease (OND, n = 33); and 4) MS patients before and after one year of treatment with natalizumab (n = 30).
  
  
  RESULTS
  Carriers of the GG genotype had the lowest serum levels of LIGHT (p=0.02). Serum levels of LIGHT were increased in MS at relapse in two separate cohorts: vs. healthy controls (p=0.00005) and vs. remission (p=0.00006), other neurological disease (OND) (p=0.002) and OND with signs of inflammation (iOND; p=0.00005). Furthermore, serum levels of LIGHT were decreased by natalizumab treatment (p=0.001).
  
  
  CONCLUSIONS
  Soluble LIGHT is an inhibitor of T-cell activation and GG carriers of rs1077667, with the highest risk for MS, had the lowest serum levels. The increased levels of LIGHT at times of increased MS activity suggest that soluble LIGHT is protective and may act to limit inflammation.
authors.affiliation: Department of Neurology, Sahlgrenska Academy at University of Gothenburg, Sweden.
authors.forename: Clas
authors.initials: C
authors.lastname: Malmeström
authors.forename: Alan
authors.initials: A
authors.lastname: Gillett
authors.forename: Margareta
authors.initials: M
authors.lastname: Jernås
authors.forename: Mohsen
authors.initials: M
authors.lastname: Khademi
authors.forename: Markus
authors.initials: M
authors.lastname: Axelsson
authors.forename: Ingrid
authors.initials: I
authors.lastname: Kockum
authors.forename: Niklas
authors.initials: N
authors.lastname: Mattsson
authors.forename: Henrik
authors.initials: H
authors.lastname: Zetterberg
authors.forename: Kaj
authors.initials: K
authors.lastname: Blennow
authors.forename: Lars
authors.initials: L
authors.lastname: Alfredsson
authors.forename: Hans
authors.initials: H
authors.lastname: Wadenvik
authors.forename: Jan
authors.initials: J
authors.lastname: Lycke
authors.forename: Tomas
authors.initials: T
authors.lastname: Olsson
authors.forename: Bob
authors.initials: B
authors.lastname: Olsson
mesh_terms: D000328:Adult; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D020022:Genetic Predisposition to Disease / Q000235:genetics*; D055106:Genome-Wide Association Study; D005838:Genotype; D006801:Humans; D008297:Male; D009103:Multiple Sclerosis / Q000097:blood* / Q000235:genetics*; D020641:Polymorphism, Single Nucleotide; D053326:Tumor Necrosis Factor Ligand Superfamily Member 14 / Q000097:blood* / Q000235:genetics*
chemical_list: C505914:TNFSF14 protein, human; D053326:Tumor Necrosis Factor Ligand Superfamily Member 14