CSL362 potently and specifically depletes pDCs in vitro and ablates SLE-immune complex-induced IFN responses

Katherine A. Monaghan, Alberta Hoi, Cristina Gamell, Tsin Yee Tai, Bryan Linggi, Jarrat Jordan, Matteo Cesaroni, Takahiro Sato, Milica Ng, Shereen Oon, Jacqueline Benson, Ian Wicks, Eric Morand, Nicholas Wilson

Research output: Contribution to journalArticleResearchpeer-review

5 Citations (Scopus)

Abstract

Systemic lupus erythematosus (SLE) is an autoimmune disease with significant morbidity and mortality. Type I interferon (IFN) drives SLE pathology and plasmacytoid dendritic cells (pDCs) are potent producers of IFN; however, the specific effects of pDC depletion have not been demonstrated. We show CD123 was highly expressed on pDCs and the anti-CD123 antibody CSL362 potently depleted pDCs in vitro. CSL362 pre-treatment abrogated the induction of IFNα and IFN-induced gene transcription following stimulation with SLE patient-derived serum or immune complexes. RNA transcripts induced in pDCs by ex vivo stimulation with TLR ligands were reflected in gene expression profiles of SLE blood, and correlated with disease severity. TLR ligand-induced protein production by SLE patient peripheral mononuclear cells was abrogated by CSL362 pre-treatment including proteins over expressed in SLE patient serum. These findings implicate pDCs as key drivers in the cellular activation and production of soluble factors seen in SLE.

Original languageEnglish
Article number107173
Number of pages22
JournaliScience
Volume26
Issue number7
DOIs
Publication statusPublished - 21 Jul 2023

Keywords

  • Health sciences
  • Immunology
  • Pathophysiology

Cite this