Interleukin-36 upregulates type-I interferon responses in systemic lupus erythematosus by promoting the accumulation of self-nucleic acids

We find that IL-36 promotes monocyte apoptosis while downregulating self-nucleic acid clearance. Thus, IL-36 contributes to the accumulation of self-nucleic acids, a key driver of type I IFN responses in SLE.

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Publication Details

Journal
Frontiers in Immunology
Published
2026-01-13
DOI
https://doi.org/10.3389/fimmu.2025.1727524
Primary Topic
Psoriasis: Treatment and Pathogenesis
Type
article
Field-Weighted Citation Impact
0.00

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article

Interleukin-36 upregulates type-I interferon responses in systemic lupus erythematosus by promoting the accumulation of self-nucleic acids

Daniel McCluskey, Myles Lewis, Emma J. Welsh, Francesca Capon et al.
Frontiers in Immunology
Psoriasis: Treatment and Pathogenesis
article

Interleukin-36 upregulates type-I interferon responses in systemic lupus erythematosus by promoting the accumulation of self-nucleic acids

Daniel McCluskey, Myles Lewis, Emma J. Welsh, Francesca Capon, Patrick Baum
article en

Abstract

We find that IL-36 promotes monocyte apoptosis while downregulating self-nucleic acid clearance. Thus, IL-36 contributes to the accumulation of self-nucleic acids, a key driver of type I IFN responses in SLE.

Frontiers in ImmunologyVol. 16
Boehringer Ingelheim (Germany) (DE), University of British Columbia (CA), Queen Mary University of London (GB), King's College London (GB), Barts Health NHS Trust (GB), BC Children's Hospital (CA)
National Institute for Health and Care Research, King's College London, Leading Edge Endowment Fund, Versus Arthritis, Barts Health NHS Trust, Medical Research Council
Openalex Percentile: Top 89%
Psoriasis: Treatment and Pathogenesis
DOIOpen Access PDFOpenAlex
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