The DOI matches its Crossref record; 87 of the 88 references it cites were found in a registry or an index.
Erythroid mitochondrial retention triggers myeloid-dependent type I interferon in human SLE
Open accessAbstract
Emerging evidence supports that mitochondrial dysfunction contributes to systemic lupus erythematosus (SLE) pathogenesis. Here we show that programmed mitochondrial removal, a hallmark of mammalian erythropoiesis, is defective in SLE. Specifically, we demonstrate that during human erythroid cell maturation, a hypoxia-inducible factor (HIF)-mediated metabolic switch is responsible for the activation of the ubiquitin-proteasome system (UPS), which precedes and is necessary for the autophagic removal of mitochondria. A defect in this pathway leads to accumulation of red blood cells (RBCs) carrying mitochondria (Mito+ RBCs) in SLE patients and in correlation with disease activity. Antibody-mediated internalization of Mito+ RBCs induces type I interferon (IFN) production through activation of cGAS in macrophages. Accordingly, SLE patients carrying both Mito+ RBCs and opsonizing antibodies display the highest levels of blood IFN-stimulated gene (ISG) signatures, a distinctive feature of SLE.
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“Abnormal retention of mitochondria in mature erythrocytes in patients with SLE is caused by a defective hypoxia-inducible factor (HIF)-mediated metabolic switch that leads to impaired activation of the ubiquitin-proteasome system, necessary for the execution of mitophagy during human erythroid cell maturation”
From The role of mitochondria in rheumatic diseases (2022) · cites this paper as [119]
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“high interferon-stimulated gene signatures in patients with SLE are associated with the presence of mitochondria-containing erythrocytes and opsonizing antibodies119”
From The role of mitochondria in rheumatic diseases (2022) · cites this paper as [119]
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“phagocytosis of opsonized mitochondria-containing erythrocytes induces activation of the DNA-sensing cyclic GMP-AMP synthase–stimulator of interferon genes (cGAS–STING) pathway in macrophages and induces subsequent production of type I interferons119”
From The role of mitochondria in rheumatic diseases (2022) · cites this paper as [119]
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“a study published in 2021 revealed that a proportion of erythrocytes contain mitochondria in SLE119”
From The role of mitochondria in rheumatic diseases (2022) · cites this paper as [119]
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1 retracted
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Items 201–228 of 228
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Metadata
- Authors
- Caielli, S., Cardenas, J., de Jesus, A. A., Baisch, J., Walters, L., Blanck, J. P., Balasubramanian, P., Stagnar, C., Ohouo, M., Hong, S., Nassi, L., Stewart, K., Fuller, J., Gu, J., Banchereau, J. F., Wright, T., Goldbach-Mansky, R., & Pascual, V.
- Affiliations
- Weill Cornell Medicine (US)
- Texas Scottish Rite Hospital for Children (US)
- The Jackson Laboratory for Genomic Medicine (US)
- Corresponding author
- Caielli, Simone
- Pascual, Virginia
- ORCID
- Venue
- Cell
- Publisher
- Elsevier BV
- Published
- 2021-08
- Volume
- 184
- Issue
- 17
- Pages
- 4464-4479.e19
- ISSN
- 0092-8674 (ISSN-L)
- PMC
- PMC8380737
- OpenAlex
- W3189265697
- Cited by
- 228
- References
- 88
- Citations by year
- 2026: 36 · 2025: 53 · 2024: 60 · 2023: 40 · 2022: 33 · 2021: 6
- FWCI
- 26.18
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- www.elsevier.com/tdm/userlicense/1.0/ (tdm)
- www.elsevier.com/legal/tdmrep-license (tdm)
- www.elsevier.com/open-access/userlicense/1.0/ (vor, 384 d)
- doi.org/10.15223/policy-017 (stm-asf)
- doi.org/10.15223/policy-037 (stm-asf)
- doi.org/10.15223/policy-012 (stm-asf)
- doi.org/10.15223/policy-029 (stm-asf)
- doi.org/10.15223/policy-004 (stm-asf)
- Locations
- Cell (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- The Mouseion at the JAXlibrary (Jackson Laboratory) (submittedVersion)
- Funders
- NIH (U19 AI082715)
- Sanofi
- AstraZeneca
- Weill Cornell Medical College
- National Institute of Allergy and Infectious Diseases
- Lupus Research Alliance
- National Institute of Arthritis and Musculoskeletal and Skin Diseases
- Topics
- Health Sciences › Medicine › Rheumatology › Systemic Lupus Erythematosus Research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Autophagy in Disease and Therapy
- Life Sciences › Immunology and Microbiology › Immunology › interferon and immune responses
- Keywords
- systemic lupus erythematosus, erythropoiesis, autophagy, hypoxia-inducible factor, ubiquitin-proteasome system, mitochondrial dysfunction, type I interferon, cGAS, macrophages, opsonic antibodies, interferon-stimulated genes, disease activity
- MeSH terms
- Endothelial PAS Domain-Containing Protein 1, Adolescent, Child, Child, Preschool, Erythroblasts, Erythrocytes, Erythropoiesis, Humans, Interferon Type I, Lupus Erythematosus, Systemic, Mitochondria, Myeloid Cells, Ubiquitin, Proteasome Endopeptidase Complex, Basic Helix-Loop-Helix Transcription Factors, Basic Helix-Loop-Helix Proteins, Mitophagy
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