ArticleClinical immunology (Orlando, Fla.)2008
A role for Fli-1 in B cell proliferation: implications for SLE pathogenesis.
Article in Clinical immunology (Orlando, Fla.), 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
20 citing papers in PubMed, 31 citations in OpenAlex.
- Biphasic control of the B cell transcriptome by mTORC1 and GSK3.Cell reports · 2025Article
- Role of Transcription Factor Fli-1 in Inflammation and Autoimmune Diseases.Biomolecules · 2025Review
- Transglutaminases are oncogenic biomarkers in human cancers and therapeutic targeting of TGM2 blocks chemoresistance and macrophage infiltration in pancreatic cancer.Cellular oncology (Dordrecht, Netherlands) · 2023Article
- Immunological Evaluation of Patients Affected with Jacobsen Syndrome Reveals Profound Not Age-Related Lymphocyte Alterations.Journal of clinical immunology · 2022Article
- Identification of diterpenoid compounds that interfere with Fli-1 DNA binding to suppress leukemogenesis.Cell death & disease · 2019Article
- Article
- Automatic identification of informative regions with epigenomic changes associated to hematopoiesis.Nucleic acids research · 2017Article
- Genome-Wide Identification of Target Genes for the Key B Cell Transcription FactorFrontiers in immunology · 2017Article
- Acetylation impacts Fli-1-driven regulation of granulocyte colony stimulating factor.European journal of immunology · 2016Article
- Fli-1, a Functional Factor Performed in Autoimmune Lupus.Inflammation · 2016Article
- Review
- Fli-1 controls transcription from the MCP-1 gene promoter, which may provide a novel mechanism for chemokine and cytokine activation.Molecular immunology · 2015Article
- The Fli-1 transcription factor regulates the expression of CCL5/RANTES.Journal of immunology (Baltimore, Md. : 1950) · 2014Article
- The transcription factor Fli-1 regulates monocyte, macrophage and dendritic cell development in mice.Immunology · 2013Article
- Article
- The transcription factor Bright plays a role in marginal zone B lymphocyte development and autoantibody production.Molecular immunology · 2011Article
- Impact of Fli-1 transcription factor on autoantibody and lupus nephritis in NZM2410 mice.Clinical and experimental immunology · 2010Article
- The impact of Fli1 deficiency on the pathogenesis of systemic sclerosis.Journal of dermatological science · 2010Review
- Altered expression of signalling lymphocyte activation molecule (SLAM) family receptors CS1 (CD319) and 2B4 (CD244) in patients with systemic lupus erythematosus.Clinical and experimental immunology · 2010Article
- Decreased expression of Fli-1 in bone marrow-derived haematopoietic cells significantly affects disease development in Murphy Roths Large/lymphoproliferation (MRL/lpr) mice.Clinical and experimental immunology · 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
5 authors at 1 institution in 1 country.
Funding
Abstract
Transgenic overexpression of Fli-1 in normal mice leads to SLE-like disease and increased expression was reported in SLE-affected human and murine lymphocytes. Reducing Fli-1 expression in MRL/lpr mice decreased antibody production, proteinuria, renal pathology, and mortality. Compared to those with wild-type expression of Fli-1, we report here that proliferative responses of Fli-1-deficient naïve B cells to several mitogens were reduced in lupus-prone and control mice. Expression of mitogen receptors, including BCR, TLR4, and TLR9, was not significantly impacted in Fli-1-deficient naïve B cells. IL12a transcripts were upregulated and NFAT transcripts were downregulated in Fli-1-deficient MRL/lpr B cells. These results demonstrate that Fli-1 deficiency affects B cell proliferative responses to mitogens, independent of BCR and TLR expression. IL12a and NFAT, known to influence proliferation, were identified as potential mediators of this effect. This may be a mechanism by which overexpression of Fli-1 contributes to B cell hyperactivity and subsequent SLE pathogenesis.
Indexed as
Identifiers
What OpenQuestion holds
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.