Identification and functional characterization of a highly polymorphic region in the human TRAIL promoter in multiple sclerosis

Publikation: Beitrag in Fachzeitschrift › Forschungsartikel › Beigetragen › Begutachtung

Beitragende

  • Alexandra Weber - , Charité – Universitätsmedizin Berlin (Autor:in)
  • Klaus Peter Wandinger - , Charité – Universitätsmedizin Berlin (Autor:in)
  • Wolf Mueller - , Charité – Universitätsmedizin Berlin (Autor:in)
  • Orhan Aktas - , Charité – Universitätsmedizin Berlin (Autor:in)
  • Oliver Wengert - , Charité – Universitätsmedizin Berlin (Autor:in)
  • Eva Grundström - , Charité – Universitätsmedizin Berlin (Autor:in)
  • Stefan Ehrlich - , Charité – Universitätsmedizin Berlin (Autor:in)
  • Christine Windemuth - , Universität Bonn (Autor:in)
  • Tanja Kuhlmann - , Centre Universitaire de Sante McGill (Autor:in)
  • Thomas Wienker - , Universität Bonn (Autor:in)
  • Wolfgang Brück - , Charité – Universitätsmedizin Berlin, Georg-August-Universität Göttingen (Autor:in)
  • Frauke Zipp - , Charité – Universitätsmedizin Berlin (Autor:in)

Abstract

TNF-related apoptosis-inducing ligand (TRAIL) is not only involved in cell death but also in other immunoregulatory mechanisms. So far, the regulation of the TRAIL pathway in physiologic and pathologic conditions remains unclear. Due to the implication in brain damage and the elevated expression in peripheral immune cells of patients with multiple sclerosis (MS), an autoimmune disease of the central nervous system, TRAIL might play a central role in the pathology of this disease. Here, we have identified a highly polymorphic region in the TRAIL promoter. Using single-strand conformation polymorphism analysis, we found four single nucleotide polymorphisms (SNPs) within 111 base pairs. One of these SNPs is located in a binding site for the transcription factor AP-1. However, the RNA and protein expression of TRAIL revealed no obvious differences in relation to the genotypes. Furthermore, investigating samples from both MS patients and healthy controls we could not detect any association of these newly described polymorphisms to the clinical disease pattern. Thus, the TRAIL promoter contains a highly polymorphic area which has, however, no impact on molecule expression, and is neither directly related to increased risk of developing MS nor associated with a certain course of this heterogeneous disease in our population.

Details

OriginalspracheEnglisch
Seiten (von - bis)195-201
Seitenumfang7
FachzeitschriftJournal of neuroimmunology
Jahrgang149
Ausgabenummer1-2
PublikationsstatusVeröffentlicht - Apr. 2004
Peer-Review-StatusJa
Extern publiziertJa

Externe IDs

PubMed 15020080
ORCID /0000-0003-2132-4445/work/202353718

Schlagworte

ASJC Scopus Sachgebiete

  • Immunologie und Allergologie - Central nervous system, CNS, EDSS, Expanded Disability Status Scale, HLA, Human leukocyte antigen, Immunogenetics, MS, Multiple sclerosis, PCR, Polymerase chain reaction, RFLP, Single nucleotide polymorphisms, TRAIL
  • Immunologie - Central nervous system, CNS, EDSS, Expanded Disability Status Scale, HLA, Human leukocyte antigen, Immunogenetics, MS, Multiple sclerosis, PCR, Polymerase chain reaction, RFLP, Single nucleotide polymorphisms, TRAIL
  • Neurologie - Central nervous system, CNS, EDSS, Expanded Disability Status Scale, HLA, Human leukocyte antigen, Immunogenetics, MS, Multiple sclerosis, PCR, Polymerase chain reaction, RFLP, Single nucleotide polymorphisms, TRAIL
  • Klinische Neurologie - Central nervous system, CNS, EDSS, Expanded Disability Status Scale, HLA, Human leukocyte antigen, Immunogenetics, MS, Multiple sclerosis, PCR, Polymerase chain reaction, RFLP, Single nucleotide polymorphisms, TRAIL

Schlagwörter

  • Central nervous system, CNS, EDSS, Expanded Disability Status Scale, HLA, Human leukocyte antigen, Immunogenetics, MS, Multiple sclerosis, PCR, Polymerase chain reaction, RFLP, Single nucleotide polymorphisms, TRAIL