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Aberrant expression of BAFF by B lymphocytes infiltrating the salivary glands of patients with primary Sjögren's syndrome

✍ Scribed by Capucine Daridon; Valérie Devauchelle; Pascal Hutin; Rozenn Le Berre; Christine Martins-Carvalho; Boutahar Bendaoud; Maryvonne Dueymes; Alain Saraux; Pierre Youinou; Jacques-Olivier Pers


Publisher
John Wiley and Sons
Year
2007
Tongue
English
Weight
949 KB
Volume
56
Category
Article
ISSN
0004-3591

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✦ Synopsis


Abstract

Objective

To identify the cells that produce BAFF in the salivary glands of patients with primary Sjögren's syndrome (SS), and to analyze BAFF receptor expression by local T and B lymphocytes.

Methods

We used 3 methods to identify the source of BAFF: in situ hybridization of the transcripts for BAFF combined with staining of membrane markers, regular and real‐time reverse transcription–polymerase chain reaction (RT‐PCR) of cultured epithelial cells, and RT‐PCR of sorted single‐cell T and B lymphocytes eluted from salivary glands. Cells expressing TACI, BCMA, and B lymphocyte stimulator receptor 3 (BR‐3) were disclosed by combining each specific staining of the receptors with each specific staining of the cells. The function of BAFF generated by epithelial cells on B lymphocytes was determined in short‐term cocultures.

Results

Transcripts for BAFF were seen in epithelial cells and infiltrating T lymphocytes and, for the first time, were detected in local B cells. It is interesting that BR‐3 was present on these B cells but not on T cells. In contrast, TACI and, to a lesser degree, BCMA were observed on transitional B lymphocytes, whereas T lymphocytes were devoid of receptors for BAFF. Furthermore, this cytokine was shown to be functional, in that epithelial cell–bound BAFF extended the survival of normal B cells, but cell‐free BAFF released in the supernatants did not.

Conclusion

These experiments establish that in primary SS, BAFF is produced not only by epithelial cells and T cells but also by B cells. The expression of receptors for BAFF would thus allow these receptors to participate in an autocrine pattern of self‐stimulation.


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