The redundant role of plasmacytoid dendritic cells in Primary Sjögren's syndrome-Reference-Cited by-同舟云学术

The redundant role of plasmacytoid dendritic cells in Primary Sjögren's syndrome

Published:2023-11-07 Issue: Volume: Page:
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Author:

Li Rongli¹,Wu Xunyao¹,Wang Mu¹,Deng Chuiwen¹,Peng Yu¹,Zhao Lidan¹,Zhang Wen¹,Jiaxin Zhou¹,Li Mengtao¹,Zhao Yan¹,Zeng Xiaofeng¹,Fei Yunyun¹

Affiliation:

1. Peking Union Medical College Hospital

Abstract

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).

Publisher

Research Square Platform LLC

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