Scandinavian journal of gastroenterology · 2007
Elevated B cell-activating factor of the tumour necrosis factor family in coeliac disease.
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Fabris Martina, Visentini Daniela, De Re Valli, Picierno Alessia, Maieron Roberto, Cannizzaro Renato, Villalta Danilo, Curcio Francesco, De Vita Salvatore, Tonutti Elio
Аннотация
OBJECTIVE: The B cell-activating factor of the tumour necrosis factor (TNF) family (BAFF) was recently described as a critical survival factor for B cells, and its expression is increased in several autoimmune diseases. Abnormal production of BAFF disturbs immune tolerance allowing the survival of autoreactive B cells and participates in the progression of B-cell lymphomas. Coeliac disease (CD) is a common autoimmune disorder induced by gluten intake in genetically predisposed individuals, associated with autoantibody production and with an increased risk of lymphoma at follow-up. The purpose of this study was to investigate the possible implications of BAFF in CD.
MATERIAL AND METHODS: Seventy-three patients with small-bowel biopsies and laboratory-proven diagnosis of CD were included in the study. All serum samples were analysed before the start of a gluten-free diet (GFD). In 12 cases, one or more samples were analysed during follow-up of the GFD. Seventy-seven blood donors were taken as controls. Serum BAFF levels and anti-transglutaminase (a-tTG) antibodies were assessed by ELISA and endomysial antibodies by indirect immunofluorescence.
RESULTS: Serum BAFF levels appeared to be significantly more elevated in CD patients than in controls (p<0.0001) and, compared with other autoimmune diseases where BAFF is increased, a much larger percentage (80.8%) of CD patients presented BAFF levels above the normal range. In addition, serum BAFF levels were found to correlate with a-tTG antibody levels (p =0.0007) and there was a significant reduction of BAFF after introduction of a GFD.
CONCLUSIONS: BAFF may represent a possible pathogenic factor in CD. Its implications for the diagnosis, prognosis and treatment of CD should also be assessed.
MATERIAL AND METHODS: Seventy-three patients with small-bowel biopsies and laboratory-proven diagnosis of CD were included in the study. All serum samples were analysed before the start of a gluten-free diet (GFD). In 12 cases, one or more samples were analysed during follow-up of the GFD. Seventy-seven blood donors were taken as controls. Serum BAFF levels and anti-transglutaminase (a-tTG) antibodies were assessed by ELISA and endomysial antibodies by indirect immunofluorescence.
RESULTS: Serum BAFF levels appeared to be significantly more elevated in CD patients than in controls (p<0.0001) and, compared with other autoimmune diseases where BAFF is increased, a much larger percentage (80.8%) of CD patients presented BAFF levels above the normal range. In addition, serum BAFF levels were found to correlate with a-tTG antibody levels (p =0.0007) and there was a significant reduction of BAFF after introduction of a GFD.
CONCLUSIONS: BAFF may represent a possible pathogenic factor in CD. Its implications for the diagnosis, prognosis and treatment of CD should also be assessed.