title: Fas ligand expression on human nucleus pulposus cells decreases with disc degeneration processes.
abstract: BACKGROUND
  The intervertebral disc has been reported to be an immunologically privileged environment, possibly mediated by Fas ligand (FasL) expression. On the other hand, recent studies have shown the infiltration of host immune cells into the degenerated disc, which may indicate the failure of the immune-privilege feature of the disc with degeneration. However, the relationship between FasL expression and disc degeneration is still unclear. Therefore, the purpose of this study was to clarify the relationship between FasL expression and disc degeneration.
  
  
  METHODS
  Ten human degenerated disc specimens were obtained from spondylolisthesis patients and ten nondegenerated discs from idiopathic scoliosis patients during surgical procedures. Immunohistochemical staining was performed to determine the presence of FasL in cross-sections of those discs. Parts of the disc tissues were used to examine FasL expression quantitatively with Western blot analysis. To examine whether the change in FasL expression was influenced by aging, an animal study comparing the discs from young and old rats were performed using magnetic resonance imaging (MRI) and real-time polymerase chain reaction (PCR) assessment.
  
  
  RESULTS
  Nucleus pulposus cells showed strong positive staining for FasL in all specimens examined. Quantitative examination demonstrated a significant decrease in FasL expression in the degenerated group compared with the nondegenerated group (average 67.6%, P<0.05). MRI showed no significant differences in the grade of disc degeneration between young and old rats, and also no significant difference in FasL mRNA in real-time PCR assay.
  
  
  CONCLUSIONS
  The current results indicate that FasL and its potential mechanism of immunological privilege could influence the protection of the intervertebral disc against degeneration.
authors.affiliation: Department of Orthopaedic Surgery, Kobe University Graduate School of Medicine, Kobe, 650-0017, Japan.
authors.forename: Shuichi
authors.initials: S
authors.lastname: Kaneyama
authors.forename: Kotaro
authors.initials: K
authors.lastname: Nishida
authors.forename: Toru
authors.initials: T
authors.lastname: Takada
authors.forename: Teppei
authors.initials: T
authors.lastname: Suzuki
authors.forename: Takatoshi
authors.initials: T
authors.lastname: Shimomura
authors.forename: Koichiro
authors.initials: K
authors.lastname: Maeno
authors.forename: Masahiro
authors.initials: M
authors.lastname: Kurosaka
authors.forename: Minoru
authors.initials: M
authors.lastname: Doita
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D000375:Aging; D000818:Animals; D002478:Cells, Cultured; D002648:Child; D053222:Fas Ligand Protein / Q000235:genetics / Q000378:metabolism*; D006801:Humans; D007403:Intervertebral Disc / Q000166:cytology / Q000378:metabolism*; D008297:Male; D008875:Middle Aged; D012333:RNA, Messenger / Q000378:metabolism; D051381:Rats; D012600:Scoliosis / Q000378:metabolism*; D013168:Spondylolisthesis / Q000378:metabolism*
chemical_list: D053222:Fas Ligand Protein; D012333:RNA, Messenger