Increased interleukin (IL)-7R alpha expression in salivary glands of patients with primary Sjogren's syndrome is restricted to T cells and correlates with IL-7 expression, lymphocyte numbers and activity

A Bikker, AA Kruize, M Wenting, Marjan Versnel, JWJ Bijlsma, FPJG Lafeber, JAG van Roon

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Abstract

Objective To identify interleukin (IL)-7R alpha expression in the labial salivary gland (LSG) of patients with primary Sjogren's syndrome (pSS) and non-Sjogren's syndrome sicca (nSS-sicca) and to study its correlation with glandular inflammation and IL-7 expression. Methods The presence of infiltrating immune cells and IL-7R alpha cells in inflamed LSG of patients with pSS (n=12) and nSS-sicca controls (n=7) was studied by immunohistochemistry and fluorescence activated cell sorting analysis upon tissue digestion (n=15 and n=13, respectively). Additionally, the correlations of IL-7R alpha cells with hallmark disease parameters of pSS, major infiltrating inflammatory cells and IL-7 were assessed. Results In the LSG of patients with pSS increased numbers of IL-7R alpha cells were found as compared with nSS-sicca patients. IL7R alpha cells strongly correlated with the lymphocytic focus score, IL-7 expression, the decrease in percentage of IgA plasma cells and numbers of CD3 T cells, CD20 B cells, and CD1a and CD208 myeloid dendritic cells. Analysis of isolated cells from the LSG demonstrated strongly increased percentages of IL-7R alpha CD3 T cells in pSS as compared with nSS, showing abun Conclusions This study shows the presence of increased IL-7R alpha T cells in the LSG of patients with pSS and their association with the severity of sialadenitis, disease parameters and IL-7 expression. Considering the immunostimulatory ability of IL-7R alpha T cells and IL-7, this suggests that IL-7(R)-dependent T cell-driven immune activation plays an important role in inflammation in pSS.
Original languageUndefined/Unknown
Pages (from-to)1027-1033
Number of pages7
JournalAnnals of the Rheumatic Diseases
Volume71
Issue number6
DOIs
Publication statusPublished - 2012

Research programs

  • EMC MM-02-72-02

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