Literature DB >> 22001522

In Sjögren's syndrome, B lymphocytes induce epithelial cells of salivary glands into apoptosis through protein kinase C delta activation.

Marie-Michèle Varin1, Thomas Guerrier, Valérie Devauchelle-Pensec, Christophe Jamin, Pierre Youinou, Jacques-Olivier Pers.   

Abstract

Sjögren's syndrome (SS) is a chronic autoimmune epithelitis associated with diffuse lymphocytic infiltration that varies in composition and differs according to lesion severity. T lymphocytes have been viewed as competent in their own right in the destruction of epithelial cells, whereas B lymphocytes that predominate in severe lesions have never been implicated in direct tissue damage. Using co-culture experiments with human salivary gland (HSG) cell line cells and tonsilar B lymphocytes, we observed that direct HSG cell-B lymphocyte contacts were able to induce apoptosis in epithelial cells. This B lymphocyte-mediated cell death could not be ascribed to Fas-Fas ligand interactions but required translocation of protein kinase C delta (PKC δ) into the nucleus of epithelial cells. Ultimately, activation of PKCδ resulted in histone H2B phosphorylation on serine 14 and poly (ADP-ribose) polymerase cleavage. Our results suggest that B lymphocytes infiltrating the SGs of patients with SS could evoke epithelial cell apoptosis. Copyright Â
© 2011 Elsevier B.V. All rights reserved.

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Year:  2011        PMID: 22001522     DOI: 10.1016/j.autrev.2011.10.005

Source DB:  PubMed          Journal:  Autoimmun Rev        ISSN: 1568-9972            Impact factor:   9.754


  19 in total

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