Morphological basis of sensory neuropathy and neuroimmunomodulation in minor salivary glands of patients with Sjögren’s syndrome

2004 ◽  
Vol 49 (7) ◽  
pp. 529-538 ◽  
Author(s):  
B Batbayar ◽  
G Nagy ◽  
G Kövesi ◽  
T Zelles ◽  
E Fehér
Reumatismo ◽  
2016 ◽  
Vol 67 (3) ◽  
pp. 85 ◽  
Author(s):  
A. Alunno ◽  
V. Caneparo ◽  
F. Carubbi ◽  
O. Bistoni ◽  
S. Caterbi ◽  
...  

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.


1994 ◽  
Vol 37 (10) ◽  
pp. 1441-1444 ◽  
Author(s):  
Jose L. Pablos ◽  
Patricia E. Carreira ◽  
Luis Morillas ◽  
Gregoria Montalvo ◽  
Claudio Ballestin ◽  
...  

2009 ◽  
Vol 36 (12) ◽  
pp. 2694-2703 ◽  
Author(s):  
LARS MORAWIETZ ◽  
LORENA MARTINEZ-GAMBOA ◽  
SONJA SCHEFFLER ◽  
GERT HAUSDORF ◽  
ANJA DANKOF ◽  
...  

Objective.Minor salivary gland specimens were analyzed to investigate dysregulation of the proteasome system in patients with Sjögren’s syndrome (SS) and patients with sicca syndrome.Methods.Labial biopsy specimens from 17 patients with SS and 11 patients with non-autoimmunesicca syndrome were analyzed by immunohistochemistry for expression of the inducible proteasomal subunits ß1i, ß2i, and ß5i. The infiltrating subsets of lymphocytes were characterized using immunofluorescence stainings against the cell-surface markers CD20 and CD27. Two-dimensional electrophoresis and immunoblotting were used for detection of the proteasomal subunits ß1 and ß1i in peripheral blood monocyte cells. Gene expression of the constitutive subunits ß1, ß2, and ß5 and the corresponding inducible subunits ß1i, ß2i, and ß5i was further investigated at the mRNA level in small lip biopsies using real-time polymerase chain reaction.Results.The expression of ß1i in infiltrating and peripheral immune cells was altered in patients with SS compared to patients with non-autoimmune sicca syndrome and healthy controls. No significant differences were found in ß2i and ß5i expression between the same groups in small lip biopsies. Chisholm-Mason grade and ß1i expression were found to be inversely correlated (Spearman r = −0.461, p = 0.014). The phenotype and distribution of the lymphocytic infiltrate showed no differences between patients with primary and secondary SS regardless of ß1i expression.Conclusion.The proteasomal ß1i subunit is dysregulated in peripheral white blood cells and in inflammatory infiltrates of minor salivary glands in patients with SS.


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