title: Deficient Fas expression by CD4+ CCR5+ T cells in multiple sclerosis.
abstract: OBJECTIVE
  To evaluate whether T cells expressing CCR5 and CXCR3 from multiple sclerosis (MS) patients are more resistant to apoptosis.
  
  
  METHODS
  Expression of CD69, TNF-R1, Fas, FasL, bcl-2, and bax was investigated in 41 MS patients and 12 healthy controls by flow cytometry in CD4+ and CD8+ T cells expressing CCR5 and CXCR3.
  
  
  RESULTS
  In MS patients, the percentage of CD69 was increased and Fas expression decreased in CD4+ CCR5+ T cells.
  
  
  CONCLUSIONS
  The lower Fas expression in activated CD4+ CCR5+ T cells might contribute to disease pathogenesis by prolonging cell survival and favoring their migration into the CNS.
authors.affiliation: Unitat de Neuroimmunologia Clínica, Hospital Universitari Vall d'Hebron, Universitat Autònoma de Barcelona, Barcelona, Spain.
authors.forename: Eva
authors.initials: E
authors.lastname: Julià
authors.forename: Xavier
authors.initials: X
authors.lastname: Montalban
authors.forename: Hammad
authors.initials: H
authors.lastname: Al-Zayat
authors.forename: Shohreh
authors.initials: S
authors.lastname: Issazadeh-Navikas
authors.forename: Robert
authors.initials: R
authors.lastname: Goertsches
authors.forename: Roland
authors.initials: R
authors.lastname: Martin
authors.forename: Manuel
authors.initials: M
authors.lastname: Comabella
mesh_terms: D000328:Adult; D000368:Aged; D015703:Antigens, CD / Q000276:immunology / Q000378:metabolism; D000945:Antigens, Differentiation, T-Lymphocyte / Q000276:immunology / Q000378:metabolism; D017209:Apoptosis / Q000276:immunology*; D015551:Autoimmunity / Q000276:immunology; D015496:CD4-Positive T-Lymphocytes / Q000276:immunology* / Q000378:metabolism; D002470:Cell Survival / Q000276:immunology; D002634:Chemotaxis, Leukocyte / Q000276:immunology; D015536:Down-Regulation / Q000276:immunology; D053222:Fas Ligand Protein / Q000276:immunology / Q000378:metabolism; D005260:Female; D006801:Humans; D007111:Immunity, Cellular / Q000276:immunology; D037181:Lectins, C-Type; D008297:Male; D008875:Middle Aged; D009103:Multiple Sclerosis / Q000276:immunology* / Q000503:physiopathology; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000276:immunology / Q000378:metabolism; D019713:Receptors, CCR5 / Q000096:biosynthesis / Q000276:immunology*; D053199:TNF Receptor-Associated Death Domain Protein / Q000276:immunology / Q000378:metabolism; D051028:bcl-2-Associated X Protein / Q000276:immunology / Q000378:metabolism; D019014:fas Receptor / Q000276:immunology*; D000099192:CD69 Antigens
chemical_list: D015703:Antigens, CD; D000945:Antigens, Differentiation, T-Lymphocyte; D053222:Fas Ligand Protein; D037181:Lectins, C-Type; D019253:Proto-Oncogene Proteins c-bcl-2; D019713:Receptors, CCR5; D053199:TNF Receptor-Associated Death Domain Protein; D051028:bcl-2-Associated X Protein; D019014:fas Receptor; D000099192:CD69 Antigens; C481226:Tradd protein, mouse