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Absence of human parvovirus B19 DNA in myoepithelial sialadenitis of primary Sjögren’s syndrome
  1. V De Re1,
  2. S De Vita2,
  3. V Battistella1,
  4. A Marzotto1,
  5. M Libra3,
  6. G Ferraccioli2,
  7. M Boiocchi1
  1. 1Division of Experimental Oncology 1, Centro di Riferimento Oncologico, Avian, Italy
  2. 2Division of Rheumatology, DPMSC, University of Udine, Italy
  3. 3Department of Biomedical Science, Clinical Pathology and Molecular Oncology Section, University of Catania, Italy
  1. Correspondence to:
    Dr M Boiocchi, Experimental Oncology 1, Centro di Riferimento Oncologico, via Pedemontana Occidentale 12, 33081 Aviano (PN), Italy;
    mboiocchi{at}cro.it

https://doi.org/10.1136/ard.61.9.855

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    Sjögren’s syndrome (SS) is an autoimmune disease that mainly affects exocrine glands and presents as persistent dryness of the mouth and eyes owing to functional impairment of the salivary and lachrymal glands. The histological hallmark is local infiltration of lymphocytes, which play a major role in tissue damage. Although B cells represent a minority of the lymphoid infiltrates in SS tissue, they may undergo polyclonal activation and oligoclonal/monoclonal expansion, which may, in turn, predispose them to a still unidentified B cell neoplastic transformation. The process of B cell activation and expansion is presumably a consequence of a chronic, although at present unidentified, antigenic stimulus that activates specific subsets of B lymphocytes.1,2 This process resembles a germinal centre reaction, in which B cells that express the antigen receptor with …

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