Expression of SOFAT by T- and B-lineage cells may contribute to bone loss

نویسندگان

  • CHRISTIAN R. JARRY
  • ELIZABETH F. MARTINEZ
  • DAIANE C. PERUZZO
  • VANESSA CARREGARO
  • LAÍS A. SACRAMENTO
  • VERA C. ARAÚJO
  • M. NEALE WEITZMANN
  • MARCELO H. NAPIMOGA
چکیده

A novel T cell-secreted cytokine, termed secreted osteoclastogenic factor of activated T cells (SOFAT) that induces osteoclastic bone resorption in a RANKL-independent manner, has been described. Our group have previously reported that SOFAT is highly expressed in gingival tissues of patients with chronic periodontitis suggesting a putative role in the bone loss associated with periodontal disease. The aim of the present study was to identify other potential cellular sources of SOFAT in the bone resorptive lesions of patients with periodontal disease. Gingival tissues were biopsied from systemically healthy subjects without periodontal disease (n=5) and patients with chronic periodontitis (n=5), and the presence of SOFAT was analyzed by immunohistochemistry and immunofluorescence staining. The present data demonstrated marked SOFAT staining in diseased periodontal tissues that was predominantly associated with the lymphocytic infiltration of gingival tissues. Notably, in addition to CD3+ T cells, B‑lineage cells including plasma cells also exhibited strong staining for SOFAT. As SOFAT has not previously been reported in B‑lineage cells, splenic T cells and B cells were further purified from BALB/c mice and activated using CD3/CD28 and lipopolysaccharide, respectively. SOFAT was quantified by reverse transcription‑quantitative polymerase chain reaction and was shown to be significantly expressed (P<0.05) in both activated T cells and B cells compared with unstimulated cells. These data support a putative role of SOFAT in the bone loss associated with chronic periodontal disease. In addition, to the best of our knowledge, this study demonstrates for the first time that in addition to T cells, B-lineage cells may also be a significant source of SOFAT in inflammatory states.

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عنوان ژورنال:

دوره 13  شماره 

صفحات  -

تاریخ انتشار 2016