ReviewImmunology letters2010
Systemic lupus erythematosus and increased risk to develop B cell malignancies: role of the p200-family proteins.
Review in Immunology letters, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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.
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Who cites it
15 citing papers in PubMed, 30 citations in OpenAlex.
- The molecular mechanisms and therapeutic potential of p53 in kidney injury repair: a perspective on the p53alpha/delta133p53alpha signaling axis.Renal failure · 2025Review
- Comparative time-series analyses of gut microbiome profiles in genetically and chemically induced lupus-prone mice and the impacts of fecal transplantation.Scientific reports · 2024Article
- A Review of the Potential Benefits of Herbal Medicines, Small Molecules of Natural Sources, and Supplements for Health Promotion in Lupus Conditions.Life (Basel, Switzerland) · 2023Review
- Interferon-induced protein 16 expression in colorectal cancer and its correlation with proliferation and immune signature markers.Oncology letters · 2021Article
- Increased expression of IFI16 predicts adverse prognosis in multiple myeloma.The pharmacogenomics journal · 2021Article
- Dysregulation of Signaling Pathways Due to Differentially Expressed Genes From the B-Cell Transcriptomes of Systemic Lupus Erythematosus Patients - A Bioinformatics Approach.Frontiers in bioengineering and biotechnology · 2020Article
- A Novel Network Pharmacology Strategy to Decode Mechanism of Lang Chuang Wan in Treating Systemic Lupus Erythematosus.Frontiers in pharmacology · 2020Article
- Correlation between systemic lupus erythematosus and malignancies: a cross-sectional population-based study.Immunologic research · 2017Article
- IFI16 Expression Is Related to Selected Transcription Factors during B-Cell Differentiation.Journal of immunology research · 2015Article
- Decreased miR-26a expression correlates with the progression of podocyte injury in autoimmune glomerulonephritis.PloS one · 2014Article
- The role of interferon-β in the treatment of multiple sclerosis and experimental autoimmune encephalomyelitis - in the perspective of inflammasomes.Immunology · 2013Review
- Structures of the HIN domain:DNA complexes reveal ligand binding and activation mechanisms of the AIM2 inflammasome and IFI16 receptor.Immunity · 2012Article
- Toll-like receptor 7 stimulates the expression of Epstein-Barr virus latent membrane protein 1.PloS one · 2012Article
- Internal standard-based analysis of microarray data2--analysis of functional associations between HVE-genes.Nucleic acids research · 2011Article
- IFN-γ upregulates survivin and Ifi202 expression to induce survival and proliferation of tumor-specific T cells.PloS one · 2010Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Systemic lupus erythematosus (SLE), an autoimmune disease, develops at a female-to-male ratio of 10:1. Increased serum levels of type I interferons (IFN-alpha/beta) and induction of "IFN-signature" genes are associated with an active SLE disease in patients. Moreover, SLE patients exhibit three- to four-fold increase in the risk of developing malignancies involving B cells, including non-Hodgkin lymphoma (NHL) and Hodgkin's lymphoma (HL). Interestingly, homozygous mice expressing a deletion mutant (the proline-rich domain deleted) of the p53 develop various types of spontaneous tumors, particularly of B cell origin upon aging. The deletion is associated with defects in transcriptional activation of genes by p53 and inhibition of DNA damage-induced apoptosis. Notably, increased levels of the p202 protein, which is encoded by the p53-repressible interferon-inducible Ifi202 gene, in B cells of female mice are associated with defects in B cell apoptosis, inhibition of the p53-mediated transcription of pro-apoptotic genes, and increased lupus susceptibility. In this review we discuss how increased levels of the p202 protein (and its human functional homologue IFI16 protein) in B cells increase lupus susceptibility and are likely to increase the risk of developing certain B cell malignancies. A complete understanding of the molecular mechanisms that regulate B cell homeostasis is necessary to identify SLE patients with an increased risk to develop B cell malignancies.
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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.