ReviewAnnals of the New York Academy of Sciences2015
Contribution of B-1a cells to systemic lupus erythematosus in the NZM2410 mouse model.
Review in Annals of the New York Academy of Sciences, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 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
11 citing papers in PubMed, 13 citations in OpenAlex.
- A novel murine model of Sjögren's disease using lacrimal autoantigen.Frontiers in immunology · 2026Article
- Article
- High throughput sequencing revealed enhanced cell cycle signaling in SLE patients.Scientific reports · 2023Article
- The Role of B1 Cells in Systemic Lupus Erythematosus.Frontiers in immunology · 2022Review
- Alpha 1 Antitrypsin Gene Therapy Extends the Lifespan of Lupus-Prone Mice.Molecular therapy. Methods & clinical development · 2018Article
- CD3+ B-1a Cells as a Mediator of Disease Progression in Autoimmune-Prone Mice.Mediators of inflammation · 2018Article
- Dysregulated Lymphoid Cell Populations in Mouse Models of Systemic Lupus Erythematosus.Clinical reviews in allergy & immunology · 2017Review
- Irgm1 coordinately regulates autoimmunity and host defense at select mucosal surfaces.JCI insight · 2017Article
- Metabolic Factors that Contribute to Lupus Pathogenesis.Critical reviews in immunology · 2016Review
- Expansion of B-1a Cells with Germline Heavy Chain Sequence in Lupus Mice.Frontiers in immunology · 2016Article
- Genetic and cellular dissection of the activation of AM14 rheumatoid factor B cells in a mouse model of lupus.Journal of leukocyte biology · 2015Article
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) is an autoimmune disease of complex etiology in which B cells play a central role. An expanded number of B-1a cells have been consistently associated with murine lupus, and more recently with human SLE. We have identified Cdkn2c, a gene that controls cell cycle progression, as a key regulator of B-1a cell numbers and have associated Cdkn2c deficiency with autoimmune pathology, including the production of autoantibodies and the skewing of CD4(+) T cells toward inflammatory effector functions. We review the genetic studies that have led to these findings, as well as the possible mechanisms by which B-1a cell expansion and Cdkn2c deficiency are related to SLE pathogenesis.
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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.