The DOI matches its Crossref record; 224 of the 224 references it cites were found in a registry or an index.
Pathogenesis of systemic lupus erythematosus: risks, mechanisms and therapeutic targets
Open accessAbstract
Research elucidating the pathogenesis of systemic lupus erythematosus (SLE) has defined two critical families of mediators, type I interferon (IFN-I) and autoantibodies targeting nucleic acids and nucleic acid-binding proteins, as fundamental contributors to the disease. On the fertile background of significant genetic risk, a triggering stimulus, perhaps microbial, induces IFN-I, autoantibody production or most likely both. When innate and adaptive immune system cells are engaged and collaborate in the autoimmune response, clinical SLE can develop. This review describes recent data from genetic analyses of patients with SLE, along with current studies of innate and adaptive immune function that contribute to sustained IFN-I pathway activation, immune activation and autoantibody production, generation of inflammatory mediators and tissue damage. The goal of these studies is to understand disease mechanisms, identify therapeutic targets and stimulate development of therapeutics that can achieve improved outcomes for patients.
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1 retracted
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RetractedAn Expanded View of Complex Traits: From Polygenic to Omnigenic
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Mitochondrial DNA stress primes the antiviral innate immune response
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Interferon and Granulopoiesis Signatures in Systemic Lupus Erythematosus Blood
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Chromatin–IgG complexes activate B cells by dual engagement of IgM and Toll-like receptors
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Impairment of neutrophil extracellular trap degradation is associated with lupus nephritis
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Homozygous C1q deficiency causes glomerulonephritis associated with multiple apoptotic bodies
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Cited by
NF-κB in biology and targeted therapy: new insights and translational implications
Guo, Q., Jin, Y., Chen, X., Ye, X., Shen, X., Lin, M., Zeng, C., Zhou, T., & Zhang, J. (2024) · Signal Transduction and Targeted Therapy · doi:10.1038/s41392-024-01757-9 · Cited by 2,047
Hoi, A., Igel, T., Mok, C. C., & Arnaud, L. (2024) · The Lancet · doi:10.1016/s0140-6736(24)00398-2 · Cited by 399
Metadata
- Authors
- Crow, M. K.
- Venue
- Annals of the Rheumatic Diseases
- Publisher
- Elsevier BV
- Published
- 2023-08
- Volume
- 82
- Issue
- 8
- Pages
- 999-1014
- ISSN
- 0003-4967 (ISSN-L)
- OpenAlex
- W4320912323
- Cited by
- 398
- References
- 224
- FWCI
- 68.90
- Type
- journal article
- Language
- en
- Open access
- bronze
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Bibliographic data: Semantic Scholar, OpenAlex, Crossref.
Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.
