Sjögren's disease & overlap diseases

Iguratimod suppresses Tfh cell differentiation in primary Sjögren’s syndrome patients through inhibiting Akt/mTOR/STAT3 signaling

Arthritis Res TherPublished Mechanistic study

Authors' conclusion

IGU suppresses Tfh cell differentiation in pSS patients through interacting with PDK1 and suppressing Akt-mTOR-STAT3 signaling.

Study context

Population
pSS patients treated with iguratimod (IGU) for 3 months; healthy controls (in vitro)
Participants
13 pSS patients
Methodological detailsprospective
  • Prospective

Main finding

As reported in the abstract

  • Tfh, plasmablast and plasma cells suppressed by IGU treatment at 1 and 3 months
  • Tfh cell differentiation and function significantly inhibited by IGU in pSS patients and healthy controls in vitro
  • PDK1 identified as a target of IGU during Tfh cell differentiation; downstream Akt phosphorylation attenuated by IGU
  • mTORC1 activity and STAT3 phosphorylation suppressed by IGU, with downregulation of BCL6 and upregulation of PRDM1
  • Akt activator restored IGU-suppressed Tfh cell differentiation

Original publication

Iguratimod suppresses Tfh cell differentiation in primary Sjögren’s syndrome patients through inhibiting Akt/mTOR/STAT3 signaling. Arthritis Res Ther. Published 22 August 2023. doi:10.1186/s13075-023-03109-4

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