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Updated: Jan 9, 2026
Fluorescence-activated Cell Sorting for Purification of Plasmacytoid Dendritic Cells from the Mouse Bone Marrow
Published on: November 4, 2016
Dysregulated plasmacytoid dendritic cells in primary Sjögren's syndrome: normal functionality but decreased
Rongli Li1, Yimeng Jia2, Xunyao Wu3
1Department of Rheumatology and Clinical Immunology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences, Peking Union Medical College, Beijing; and Department of Rheumatology and Immunology, the First People's Hospital of Yunnan Province, the affiliated Hospital of Kunming University of Science and Technology, China.
Objectives:
Primary Sjögren's syndrome (pSS) is an autoimmune disorder characterised by type I interferons (IFNs) signature, and plasmacytoid dendritic cell (pDC) is the primary producer of type I IFNs. However, the role of pDCs in the pathogenesis of pSS remains unclear. Our study aims to explore the dysregulation of pDCs in pSS, as well as the underlying mechanisms.
Methods:
In the present study, we included a total of 104 patients with pSS (64 were untreated and 40 were treated with hydroxychloroquine) and 64 healthy controls. We examined the frequency, activation markers, cytokines secretion, and infiltration into affected tissue of pDCs derived from pSS. Clinical correlation analyses and co-culture systems of pDCs and B cells were conducted to explore the pathogenesis of pDC reduction in pSS.
Results:
The frequency of pDC was significantly reduced in the peripheral blood of pSS. pDCs derived from pSS exhibited higher expression levels of Toll-like receptor 7 in the resting state. The IFN-α production by pDCs from pSS patients is similar to that of matched HC in vitro, regardless of whether the patients' IFN signature is negative or positive. Local invasion of pDCs into affected glands was detected but not common in pSS. In pSS patients, the proportion of circulating pDCs negatively correlated with serum IgG, IgA, and anti-SSA autoantibodies. pDCs promote proliferation, activation, differentiation, and antibody production of B cells. Conversely, excessive IgG promoted pDC apoptosis via neonatal Fc receptor (FcRn) and caused the decline of pDCs in pSS.
Conclusions:
Our data enhances the understanding of pDC functionality in pSS and the mechanisms of their abnormal reduction in peripheral blood. We first report that excess IgG induced pDC apoptosis via FcRn and promoted the reduction of peripheral pDCs in patients with pSS.
