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Elevated B cell-activating factor of the tumour necrosis factor family in coeliac disease

Fabris M
•
Visentini D
•
De Re V
altro
DE VITA, Salvatore
2007
  • journal article

Periodico
SCANDINAVIAN JOURNAL OF GASTROENTEROLOGY
Abstract
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.
DOI
10.1080/00365520701452225
WOS
WOS:000250903900006
Archivio
http://hdl.handle.net/11390/880868
info:eu-repo/semantics/altIdentifier/scopus/2-s2.0-36248929907
Diritti
metadata only access
Scopus© citazioni
25
Data di acquisizione
Jun 2, 2022
Vedi dettagli
Web of Science© citazioni
23
Data di acquisizione
Mar 24, 2024
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