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
Martinez, J., Almendinger, J., Oberst, A., Ness, R., Dillon, C. P., Fitzgerald, P., Hengartner, M. O., & Green, D. R. (2011) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1113421108 · Cited by 655
RetractedMetabolic regulation of gene expression by histone lactylation
Zhang, D., Tang, Z., Huang, H., Zhou, G., Cui, C., Weng, Y., Liu, W., Kim, S., Lee, S., Perez-Neut, M., et al. (2019) · Nature · doi:10.1038/s41586-019-1678-1 · Cited by 4,371
A Cold-Inducible Coactivator of Nuclear Receptors Linked to Adaptive Thermogenesis
Puigserver, P., Wu, Z., Park, C. W., Graves, R., Wright, M., & Spiegelman, B. M. (1998) · Cell · doi:10.1016/s0092-8674(00)81410-5 · Cited by 3,864
SYSTEMIC LUPUS ERYTHEMATOSUS DISEASE ACTIVITY INDEX
Gladman, D. D., Ibañez, D., & Urowitz, M. B. (2007) · Elsevier eBooks · doi:10.1016/b978-0-323-04434-9.50060-9 · Cited by 2,928
Mitophagy and Quality Control Mechanisms in Mitochondrial Maintenance
Pickles, S., Vigié, P., & Youle, R. J. (2018) · Current Biology · doi:10.1016/j.cub.2018.01.004 · Cited by 2,081
Mitochondrial DNA stress primes the antiviral innate immune response
West, A. P., Khoury-Hanold, W., Staron, M., Tal, M. C., Pineda, C. M., Lang, S. M., Bestwick, M., Duguay, B. A., Raimundo, N., MacDuff, D. A., et al. (2015) · Nature · doi:10.1038/nature14156 · Cited by 1,975
Lood, C., Blanco, L. P., Purmalek, M. M., Carmona-Rivera, C., De Ravin, S. S., Smith, C. K., Malech, H. L., Ledbetter, J. A., Elkon, K. B., & Kaplan, M. J. (2016) · Nature Medicine · doi:10.1038/nm.4027 · Cited by 1,570
DNA sensing by the cGAS–STING pathway in health and disease
Motwani, M., Pesiridis, S., & Fitzgerald, K. A. (2019) · Nature Reviews Genetics · doi:10.1038/s41576-019-0151-1 · Cited by 1,467
Trial of Anifrolumab in Active Systemic Lupus Erythematosus
Morand, E. F., Furie, R. A., Tanaka, Y., Bruce, I. N., Askanase, A., Richez, C., Bae, S., Brohawn, P. Z., Pineda, L., Berglind, A., et al. (2019) · New England Journal of Medicine · doi:10.1056/nejmoa1912196 · Cited by 1,390
Proteasome and p97 mediate mitophagy and degradation of mitofusins induced by Parkin
Tanaka, A., Cleland, M. M., Xu, S., Narendra, D. P., Suen, D.-F., Karbowski, M., & Youle, R. J. (2010) · Journal of Cell Biology · doi:10.1083/jcb.201007013 · Cited by 1,369
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1 of the 88 references couldn’t be matched to a known paper.
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Lactate metabolism in human health and disease
Li, X., Yang, Y., Zhang, B., Lin, X., Fu, X., An, Y., Zou, Y., Wang, J.-X., Wang, Z., & Yu, T. (2022) · Signal Transduction and Targeted Therapy · doi:10.1038/s41392-022-01151-3 · Cited by 1,454
Mitochondrial control of inflammation
Marchi, S., Guilbaud, E., Tait, S. W. G., Yamazaki, T., & Galluzzi, L. (2023) · Nature Reviews Immunology · doi:10.1038/s41577-022-00760-x · Cited by 1,027
Mitochondrial DNA Release in Innate Immune Signaling
Newman, L. E., & Shadel, G. S. (2023) · Annual Review of Biochemistry · doi:10.1146/annurev-biochem-032620-104401 · Cited by 349
Role of the cGAS–STING pathway in systemic and organ-specific diseases
Skopelja‐Gardner, S., An, J., & Elkon, K. B. (2022) · Nature Reviews Nephrology · doi:10.1038/s41581-022-00589-6 · Cited by 318
Systemic Lupus Erythematosus Pathogenesis: Interferon and Beyond
Caielli, S., Wan, Z., & Pascual, V. (2023) · Annual Review of Immunology · doi:10.1146/annurev-immunol-101921-042422 · Cited by 229
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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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