Ductal epithelial expression of R o52 correlates with inflammation in salivary glands of patients with primary S jögren's syndrome
Author(s) -
Aqrawi L. A.,
Kvarnström M.,
Brokstad K. A.,
Jonsson R.,
Skarstein K.,
WahrenHerlenius M.
Publication year - 2014
Publication title -
clinical & experimental immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.329
H-Index - 135
eISSN - 1365-2249
pISSN - 0009-9104
DOI - 10.1111/cei.12341
Subject(s) - saliva , autoantibody , immunohistochemistry , inflammation , salivary gland , pathology , antibody , ductal cells , biology , immunology , medicine
Summary R o52 is an E 3 ubiquitin ligase with a prominent regulatory role in inflammation. The protein is a common target of circulating autoantibodies in rheumatic autoimmune diseases, particularly S jögren's syndrome ( SS ). In this study we aimed to investigate the expression of the SS target autoantigen R o52 in salivary glands of patients with primary S jögren's syndrome (p SS ). R o52 expression was assessed by immunohistochemical staining of paraffin‐embedded and frozen salivary gland biopsies from 28 p SS patients and 19 non‐p SS controls from S wedish and N orwegian registries, using anti‐human R o52 monoclonal antibodies. The degree and pattern of staining and inflammation was then evaluated. Furthermore, secreted R o52 protein was measured in saliva and serum samples from the same individuals through a catch‐enzyme‐linked immunosorbent assay ( ELISA) . R o52 was highly expressed in all the focal infiltrates in p SS patients. Interestingly, a significantly higher degree of R o52 expression in ductal epithelium was observed in the patients compared to the non‐p SS controls ( P < 0·03). Moreover, the degree of ductal epithelial expression of R o52 correlated with the level of inflammation ( S pearman's r = 0·48, P < 0·0120). However, no secreted R o52 protein could be detected in serum and saliva samples of these subjects. R o52 expression in ductal epithelium coincides with degree of inflammation and is up‐regulated in p SS patients. High expression of R o52 might result in the breakage of tolerance and generation of R o52 autoantibodies in genetically susceptible individuals. We conclude that the up‐regulation of R o52 in ductal epithelium might be a triggering factor for disease progression in SS .
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