ReviewNature reviews. Rheumatology2010
The role of defective clearance of apoptotic cells in systemic autoimmunity.
Review in Nature reviews. Rheumatology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 322 papers, 2 of them syntheses that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
322 citing papers in PubMed, 2 syntheses or guidelines pooled it.
- Ficolin-3 Deficiency Is Associated with Disease and an Increased Risk of Systemic Lupus Erythematosus.Journal of clinical immunology · 2019Pooled it
- Systemic Lupus Erythematosus and DNA Degradation and Elimination Defects.Frontiers in immunology · 2019Pooled it
- Clearance of apoptotic cells by mesenchymal stem cells contributes to immunosuppression via PGE2.EBioMedicine · 2019Trial
- Immune cell-derived membrane nanovesicles: A promethean fire for autoimmune disease therapy through immune cell mimicry.Bioactive materials · 2026Review
- Electrostatic control of chromatin compaction safeguards against apoptotic DNA release.The EMBO journal · 2026Article
- Disease modification in lupus nephritis: towards a pathophysiology-based treatment paradigm.Nature reviews. Nephrology · 2026Review
- Article
- Dysregulation of the DNA repair‑immune axis: Targeted therapeutic strategies for autoimmune diseases (Review).International journal of molecular medicine · 2026Review
- dsDNA-Induced AIM2 Pyroptosis in Glomerular Endothelial Cells Aggravate Lupus Nephritis.Cell biochemistry and biophysics · 2026Article
- From Genes to Pathways: The Molecular Landscape of Systemic Lupus Erythematosus.International journal of molecular sciences · 2026Review
- Review
- Identification of key programmed cell death genes-necroptosis-related genes in systemic lupus erythematosus.Clinical and experimental medicine · 2026Article
- The emerging role of TLR7-mediated signaling in respiratory viral infections and autoimmune diseases.Cellular and molecular life sciences : CMLS · 2026Review
- Neutrophils as critical orchestrators of chronic inflammation.Cellular & molecular immunology · 2026Review
- Autoantibodies as Precision Tools in Connective Tissue Diseases: From Epiphenomenon to Endophenotype.Antibodies (Basel, Switzerland) · 2026Review
- Hormone-sensitive lipase drives pro-resolving macrophage polarization and enhances efferocytosis.Cell communication and signaling : CCS · 2026Article
- Cell-free DNA fragmentation signatures link cancer and autoimmunity.Nature reviews. Rheumatology · 2026Article
- Renal macrophage TLR7 signaling in lupus nephritis: from pathogenic mechanisms to therapeutic opportunities.Frontiers in immunology · 2026Review
- TLR7 and TLR9 have overlapping but distinct roles in systemic lupus erythematosus and Sjögren's disease.Frontiers in immunology · 2026Review
- Case Report: Transient immune dysregulation in early infancy mimicking severe systemic autoimmunity with complete spontaneous resolution.Frontiers in immunology · 2026Article
262 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The inefficient clearance of dying cells can result in the accumulation of apoptotic cell remnants. This occurrence is considered an intrinsic defect that can cause the permanent presence of cellular debris responsible for the initiation of systemic autoimmunity in diseases such as systemic lupus erythematosus (SLE). If postapoptotic debris accumulates in germinal centers, activates complement and functions as a survival signal for B cells that have become autoreactive by somatic hypermutation, autoimmunity could arise (etiology). The accumulation of postapoptotic remnants and fragments derived from secondary necrotic cells in the presence of autoantibodies against apoptotic cells or adaptor molecules obliges their pathological elimination and maintains autoinflammation. The autoimmunity that occurs in patients with SLE involves complex antigens that contain nucleic acids, which can function as virus mimetics. Complexes of autoantibodies, proteins and nucleic acids are likely to be mistaken by the immune system for opsonized viruses, resulting in the production of type I interferons, a hallmark of SLE (pathogenesis). The pathogenicity of autoantibodies is thought to strongly increase if autoantigens are accessible for immune-complex formation. The immune complex could be considered a binary pyrogen formed from less proinflammatory components. The accessibility of cognate autoantigens, in turn, is likely to be related to impaired or delayed clearance of apoptotic cells.
Indexed as
Identifiers
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.