Sjögren's disease & overlap diseases

Dysregulated plasmacytoid dendritic cells in primary Sjögren's syndrome: normal functionality but decreased quantities

Clin Exp RheumatolPublished Mechanistic study

Authors' conclusion

We first report that excess IgG induced pDC apoptosis via FcRn and promoted the reduction of peripheral pDCs in patients with pSS.

Study context

Population
Patients with primary Sjögren's syndrome and healthy controls
Participants
104 vs 64
Comparison
Primary Sjögren's syndrome (pSS) vs healthy controls
  • pSSn = 104
  • HCn = 64reference
Methodological detailscase-control, in vitro co-culture of plasmacytoid dendritic cell (pDCs) and B cells
  • Case-control
  • In vitro co-culture of pDCs and B cells

Main finding

As reported in the abstract

  • pDC frequency significantly reduced in peripheral blood of pSS
  • pDCs from pSS had higher Toll-like receptor 7 expression in resting state
  • IFN-α production by pSS pDCs similar to matched HC in vitro, regardless of IFN signature
  • Local pDC invasion into affected glands detected but not common
  • Circulating pDC proportion negatively correlated with serum IgG, IgA and anti-SSA autoantibodies
  • pDCs promote B cell proliferation, activation, differentiation and antibody production
  • Excess IgG promoted pDC apoptosis via FcRn and caused pDC decline in pSS

Original publication

Dysregulated plasmacytoid dendritic cells in primary Sjögren's syndrome: normal functionality but decreased quantities. Clin Exp Rheumatol. Published 24 March 2025. doi:10.55563/clinexprheumatol/ric794

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