title: Shedding of TNF receptors in multiple sclerosis patients.
abstract: OBJECTIVE
  To evaluate the rate of shedding of tumor necrosis factor (TNF) receptors (TNFRs) in MS patients.
  
  
  BACKGROUND
  It was previously suggested that TNF might play a significant role in the immunopathologic mechanism of MS. TNF mediates its biologic effects by interacting with two distinct receptors: TNFR-p55 and TNFR-p75. Both of these receptors exist in soluble and membrane-bound forms. Soluble receptors have been shown to influence TNF activity in vitro and in vivo and maintain balance between active, free TNF and inactive form of this cytokine bound to its soluble receptors.
  
  
  METHODS
  In the current study, the authors measured shedding of TNFRs from cell surface of peripheral blood mononuclear cells, peripheral blood lymphocytes, and monocytes in three groups of MS patients: relapsing-remitting in relapse, relapsing-remitting in remission, and chronic progressive.
  
  
  RESULTS
  The authors observed a significant distortion in generation of both soluble TNF receptors. Whereas the TNFR-p55 was shed at lower rate compared with healthy volunteers, the shedding of TNFR-p75 was significantly higher in MS patients.
  
  
  CONCLUSIONS
  Disturbance in TNFR shedding might contribute to the distortion of a fine balance between circulating TNF and its natural inhibitors in MS.
authors.affiliation: Department of Neurology, Medical University of Lodz, Poland.
authors.forename: A M
authors.initials: AM
authors.lastname: Jurewicz
authors.forename: A K
authors.initials: AK
authors.lastname: Walczak
authors.forename: K W
authors.initials: KW
authors.lastname: Selmaj
mesh_terms: D015703:Antigens, CD / Q000096:biosynthesis / Q000097:blood; D002478:Cells, Cultured; D004791:Enzyme Inhibitors / Q000494:pharmacology; D006801:Humans; D007700:Kinetics; D008214:Lymphocytes / Q000378:metabolism; D009000:Monocytes / Q000187:drug effects / Q000378:metabolism; D009103:Multiple Sclerosis / Q000378:metabolism*; D011493:Protein Kinase C / Q000037:antagonists & inhibitors; D018124:Receptors, Tumor Necrosis Factor / Q000096:biosynthesis / Q000097:blood / Q000378:metabolism*; D047888:Receptors, Tumor Necrosis Factor, Type I; D047889:Receptors, Tumor Necrosis Factor, Type II; D012995:Solubility; D019311:Staurosporine / Q000494:pharmacology; D014409:Tumor Necrosis Factor-alpha / Q000096:biosynthesis
chemical_list: D015703:Antigens, CD; D004791:Enzyme Inhibitors; D018124:Receptors, Tumor Necrosis Factor; D047888:Receptors, Tumor Necrosis Factor, Type I; D047889:Receptors, Tumor Necrosis Factor, Type II; D014409:Tumor Necrosis Factor-alpha; D011493:Protein Kinase C; D019311:Staurosporine