Interferon gamma-inducible protein 16 (IFI16) and anti-IFI16 antibodies in primary Sjögren’s syndrome: findings in serum and minor salivary glands

  • A. Alunno Rheumatology Unit, Department of Medicine, University of Perugia, Perugia, Italy.
  • V. Caneparo Virology Unit, Department of Translational Medicine, Novara Medical School, Novara, Italy.
  • F. Carubbi Rheumatology Unit, Department of Biotechnological and Applied Clinical Sciences, University of L’Aquila, L’Aquila, Italy.
  • O. Bistoni Rheumatology Unit, Department of Medicine, University of Perugia, Perugia, Italy.
  • S. Caterbi Rheumatology Unit, Department of Medicine, University of Perugia, Perugia, Italy.
  • M. Gariglio Virology Unit, Department of Translational Medicine, Novara Medical School, Novara, Italy.
  • E. Bartoloni Rheumatology Unit, Department of Medicine, University of Perugia, Perugia, Italy.
  • S. Landolfo Viral Pathogenesis Unit, Department of Public Health and Pediatric Sciences, Turin Medical School, Turin, Italy.
  • R. Gerli | roberto.gerli@unipg.it Rheumatology Unit, Department of Medicine, University of Perugia, Perugia, Italy.

Abstract

The interferon (IFN) signature, namely the overexpression of IFN-inducible genes is a crucial aspect in the pathogenesis of primary Sjögren’s syndrome (pSS). The IFN-inducible IFI16 protein, normally expressed in cell nuclei, may be overexpressed, mislocalized in the cytoplasm and secreted in the extracellular milieu in several autoimmune disorders including pSS. This leads to tolerance breaking to this self-protein and development of anti-IFI16 antibodies. The aim of this study was to identify pathogenic and clinical significance of IFI16 and anti-IFI16 autoantibodies in pSS. IFI16 and anti-IFI16 were assessed in the serum of 30 pSS patients and one-hundred healthy donors (HD) by ELISA. IFI16 was also evaluated in 5 minor salivary glands (MSGs) of pSS patients and 5 MSGs of non-pSS patients with sicca symptoms by immunohistochemistry. Normal MSGs do not constitutively express IFI16. Conversely, in pSS-MSGs a marked expression and cytoplasmic mislocalization of IFI16 by epithelial cells was observed with infiltrations in lymphocytes and peri/ intra-lesional endothelium. pSS patients display higher serum levels of both IFI16 and anti-IFI16 autoantibodies compared to HD. Our data suggest that IFI16 protein may be involved in the initiation and perpetuation of glandular inflammation occurring in pSS.

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Published
2016-02-09
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Keywords:
Sjögren’s syndrome, interferons, IFI16.
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How to Cite
Alunno, A., Caneparo, V., Carubbi, F., Bistoni, O., Caterbi, S., Gariglio, M., Bartoloni, E., Landolfo, S., & Gerli, R. (2016). Interferon gamma-inducible protein 16 (IFI16) and anti-IFI16 antibodies in primary Sjögren’s syndrome: findings in serum and minor salivary glands. Reumatismo, 67(3), 85-90. https://doi.org/10.4081/reumatismo.2015.839

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