title: B cell activation in rheumatoid arthritis patients under infliximab treatment.
abstract: OBJECTIVE
  To determine whether anti-TNF alpha (infliximab) treatment affects B cell activation in patients with rheumatoid arthritis (RA) METHODS: B cell activation was analyzed in fifteen anti-TNF-treated RA patients. CD23 expression was used as a B cell activation marker and was studied before and after three months of infliximab treatment. PBMC were stimulated with anti-CD3 mAb during 18 h and were separated by rosseting into E+ and E-cells. B cells were assessed in E-population by double staining with CD19 and CD23. ELISA assays were used to assess both soluble TNF alpha and circulant immune complexes (CIC) containing TNF alpha. We also used B cells from tonsils to establish the relationship between B cell activation and TNF alpha CIC.
  
  
  RESULTS
  The proportion of B cells expressing CD23 was higher before infliximab exposure than after treatment (48.3 +/- 16.7 versus 29.5 +/- 12.5, p = 0.007). T-B cell interactions were assessed by means of blocking antibodies to CD154, CD40, CD69, and CD18; these interactions were not specially affected by infliximab treatment. We could demonstrate CIC containing TNF alpha after infliximab treatment, these CIC, similarly to others IgG-containing immune complexes, were capable to downregulate CD23 on B cells.
  
  
  CONCLUSIONS
  Infliximab treatment in RA downregulates CD23 expression on T-cell activated B cells. This downregulation is connected with the presence of CIC containing TNF alpha. Presumably, the Fc gamma RIIb1 endows IgG-containing immune complexes, as TNF alpha-anti-TNF alpha, with the capacity to regulate B cells and inflammatory cells.
authors.affiliation: Rheumatology Service, Hospital Clinico San Carlos, Madrid, Spain.
authors.forename: S
authors.initials: S
authors.lastname: De Miguel
authors.forename: J A
authors.initials: JA
authors.lastname: Jover
authors.forename: C
authors.initials: C
authors.lastname: Vadillo
authors.forename: E
authors.initials: E
authors.lastname: Judez
authors.forename: E
authors.initials: E
authors.lastname: Loza
authors.forename: B
authors.initials: B
authors.lastname: Fernandez-Gutierrez
mesh_terms: D000328:Adult; D000911:Antibodies, Monoclonal / Q000627:therapeutic use*; D001172:Arthritis, Rheumatoid / Q000175:diagnosis / Q000188:drug therapy* / Q000276:immunology*; D001402:B-Lymphocytes / Q000276:immunology* / Q000502:physiology; D015496:CD4-Positive T-Lymphocytes / Q000276:immunology / Q000378:metabolism; D023201:CD40 Ligand / Q000096:biosynthesis / Q000276:immunology; D004305:Dose-Response Relationship, Drug; D004334:Drug Administration Schedule; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D006801:Humans; D000069285:Infliximab; D008213:Lymphocyte Activation / Q000276:immunology; D008297:Male; D008875:Middle Aged; D017455:Receptors, IgE / Q000276:immunology*; D018570:Risk Assessment; D012494:Sampling Studies; D012680:Sensitivity and Specificity; D012720:Severity of Illness Index; D014409:Tumor Necrosis Factor-alpha / Q000276:immunology*
chemical_list: D000911:Antibodies, Monoclonal; D017455:Receptors, IgE; D014409:Tumor Necrosis Factor-alpha; D023201:CD40 Ligand; D000069285:Infliximab