ArticleInflammation research : official journal of the European Histamine Research Society ... [et al.]2022
IL-38, a potential therapeutic agent for lupus, inhibits lupus progression.
Article in Inflammation research : official journal of the European Histamine Research Society ... [et al.], 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 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.
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Who cites it
7 citing papers in PubMed, 12 citations in OpenAlex.
- Butyrophilin 3A1 Contributes to Inflammation and Induces a Lupus-Like Disease by Inhibiting the IL-38-Ferroptosis Axis.MedComm · 2025Article
- Enhancing the treatment potential of IL-17 antagonism in lupus nephritis: finding the right partner.Frontiers in immunology · 2025Review
- Emerging functions and therapeutic targets of IL-38 in central nervous system diseases.CNS neuroscience & therapeutics · 2024Review
- Role of IL-1 Family Cytokines IL-36, IL-37, IL-38 in Osteoarthritis and Rheumatoid Arthritis: A Comprehensive Review.Journal of inflammation research · 2024Review
- IL-38 Aggravates Atopic Dermatitis via Facilitating Migration of Langerhans cells.International journal of biological sciences · 2024Article
- IL-38 alleviates airway remodeling in chronic asthma via blocking the profibrotic effect of IL-36γ.Clinical and experimental immunology · 2023Article
- IL-38 regulates intestinal stem cell homeostasis by inducing WNT signaling and beneficial IL-1β secretion.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
backgroundPrevious studies reported that IL-38 was abnormally expressed in patients with systemic lupus erythematosus (SLE). However, the involvement of IL-38 in the pathophysiology of SLE remains unknown.
methodsThe therapeutic potential of IL-38 was tested in pristane-treated wild-type (WT) and IL-38
resultsWT mice with pristane-induced lupus exhibited hepatomegaly, splenomegaly, severe kidney damages, increased lymphoproliferation, enhanced lymphoproliferation, and upregulated inflammatory cytokines, such as IL-6, IL-13, IL-17A, MIP-3α, IL-12p70, and IFNγ, and elevated levels of autoantibodies, such as ANA IgG, anti-dsDNA IgG, and total IgG. IL-38
conclusionIL-38 regulates SLE pathogenesis. Furthermore, targeting IL-38 is critical in the treatment of SLE.
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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.