ArticleFrontiers in immunology2020
Partial Protection From Lupus-Like Disease by B-Cell Specific Type I Interferon Receptor Deficiency.
Article in Frontiers in immunology, 2020. 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
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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
11 citing papers in PubMed.
- Contribution of localmBio · 2026Article
- EGFR-ErbB2 dual kinase inhibitor lapatinib decreases autoantibody levels and worsens renal disease in Interferon α-accelerated murine lupus.International immunopharmacology · 2024Article
- Type I Interferons in Systemic Autoimmune Rheumatic Diseases: Pathogenesis, Clinical Features and Treatment Options.Mediterranean journal of rheumatology · 2024Review
- TLR7 activation of age-associated B cells mediates disease in a mouse model of primary Sjögren's disease.Journal of leukocyte biology · 2024Article
- Cutaneous Lupus Erythematosus: An Update on Pathogenesis and Future Therapeutic Directions.American journal of clinical dermatology · 2023Review
- Article
- Spontaneous CD4+ T Cell Activation and Differentiation in Lupus-Prone B6.Nba2 Mice Is IFNAR-Independent.International journal of molecular sciences · 2022Article
- Targeting type I interferons in systemic lupus erythematous.Frontiers in pharmacology · 2022Review
- Regulation of B Cell Responses in SLE by Three Classes of Interferons.International journal of molecular sciences · 2021Review
- B Cell Intrinsic STING Signaling Is Not Required for Autoreactive Germinal Center Participation.Frontiers in immunology · 2021Article
- B Cell Signatures Distinguish Cutaneous Lupus Erythematosus Subtypes and the Presence of Systemic Disease Activity.Frontiers in immunology · 2021Article
Corrections and comments
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Authors and funding
5 authors.
Funding
Abstract
Systemic lupus erythematosus (SLE) is an autoimmune disease that can present with many different permutations of symptom presentation. A large subset of SLE patients have been shown to present with elevated interferon stimulated gene (ISG) expression, and Type I IFNs (IFNαβ) have been shown to drive disease in murine models through global IFNα Receptor (IFNAR) knockouts. However, the disease contribution of distinct immune cell subsets in response to constitutively increased levels of IFNαβ is not fully understood. We utilized a B-cell specific IFNAR knockout (BΔIFNAR) on the B6.Nba2 spontaneous-lupus background to determine the contribution of IFNαβ stimulated B cells in disease. We found that IFNαβ signaling in B cells is driving increased splenomegaly, increased populations of activated B cells, and increased populations of germinal center (GC) B cells, memory B cells, and plasma blasts/cells, but did not affect the development of glomerulonephritis and immune-complex deposition. IFNAR expression by B cells also drove production of anti-chromatin IgG, and anti-dsDNA and -nRNP IgG and IgG
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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.