Lupus & antiphospholipid syndrome
Regulatory dynamics of IFI44L in systemic lupus erythematosus: the interplay of type I interferon and c-Jun
Authors' conclusion
Our research indicates that IFN-α enhances IFI44L expression via c-Jun, underscoring its critical role in the pathogenesis of SLE
Study context
- Population
- Patients with SLE (PBMC); THP-1 cells; Ifi44l knockout and Pristane-induced lupus mice
Methodological detailsin vitro THP-1 cell model overexpressing IFI44L, Ifi44l knockout mice, Pristane-induced lupus mice
- In vitro THP-1 cell model overexpressing IFI44L
- Ifi44l knockout mice
- Pristane-induced lupus mice
Main finding
As reported in the abstract
- IFI44L significantly expressed in CD3+ and CD14+ lymphocytes in SLE
- Under heightened interferon (IFN), IFI44L promotes cell proliferation and inhibits apoptosis
- Ifi44l knockout mice: ameliorated lupus features, reduced haematological and renal damage
- c-Jun directly targets the IFI44L promoter, activated by IFN-α in CD14+ lymphocytes
Original publication
Regulatory dynamics of IFI44L in systemic lupus erythematosus: the interplay of type I interferon and c-Jun. Lupus Sci Med. Published 27 January 2026. doi:10.
Composed by AI from the published abstract and checked against it. How Briefs are made →