Abstract
Objective: The aim of our present study is to investigate the
role of plasmacytoid dendritic cells (pDCs) in the pathogenesis and type
I interferon (IFN) signatures in Primary Sjögren’s Syndrome (pSS)
patients.
Methods: In the present study, we compared the percentage,
activation markers, and representative cytokines secretion of pDCs
derived from treatment-naive pSS and matched healthy controls (HCs) by
flow cytometry. We performed pDC/B co-culture system to explore the
contribution of pDC to B cell functions in pSS.
Results: The percentage of pDC was significantly reduced in the
peripheral blood of pSS. The activation markers (CD80, CD83, and CD86)
expressions, chemokine receptors, and representative cytokines
production (IFN-α, IL-6, and TNF-α) of pDC were similar between pSS and
HCs. Only a few pDCs infiltration were detected in the labial gland. The
percentage of pDCs was negatively correlated with serum IgG, IgA, and
anti-SSA autoantibody levels and resting pDCs were able to efficiently
promote B cells proliferation, activation, differentiation, and antibody
production in vitro . However, there was no difference between HC
and pSS-derived pDCs. Finally, we found that incubation of plasma from
pSS patients could significantly induce pDCs apoptosis than that from
HCs and both IgG and IgA dramatically increased the apoptotic rates of
pDCs.
Conclusion: Our data have deciphered the redundant role of pDC
in the type I signature and disease development in pSS. Also, we
demonstrated the decreased percentage of pDC in pSS patients might
result from apoptosis induced by the excess of immunoglobulin (IgG and
IgA).
Key words: Primary Sjögren’s syndrome, Plasmacytoid dendritic
cell, Type I interferon, B cell, Hypergammaglobulinemia