ArticleImmunology2019
CR6-interacting factor 1 controls autoimmune arthritis by regulation of signal transducer and activator of transcription 3 pathway and T helper type 17 cells.
Article in Immunology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers, 1 of them a synthesis that pooled it.
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
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Who cites it
8 citing papers in PubMed, 1 synthesis or guideline pooled it, 9 citations in OpenAlex.
- Association between the polymorphism of IL-17A and IL-17F gene with knee osteoarthritis risk: a meta-analysis based on case-control studies.Journal of orthopaedic surgery and research · 2019Pooled it
- Therapeutic effects of a synthetic glabridin derivative on metabolic immuno-regulation and salivary gland functional restoration in experimental Sjögren's syndrome.Experimental & molecular medicine · 2026Article
- CRIF1 gene therapy ameliorates inflammatory bowel disease by suppressing TH17 cells and fibrosis through mitochondrial function regulation.Frontiers in immunology · 2025Article
- Article
- Helper T cells: A potential target for sex hormones to ameliorate rheumatoid arthritis? (Review).Molecular medicine reports · 2024Review
- Unraveling the roles and mechanisms of mitochondrial translation in normal and malignant hematopoiesis.Journal of hematology & oncology · 2024Review
- Multifunctions of CRIF1 in cancers and mitochondrial dysfunction.Frontiers in oncology · 2022Review
- Abnormal Expression of Mitochondrial Ribosomal Proteins and Their Encoding Genes with Cell Apoptosis and Diseases.International journal of molecular sciences · 2020Review
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
CR6-interacting factor 1 (CRIF1) is a nuclear protein that interacts with other nuclear factors and androgen receptors, and is implicated in the regulation of cell cycle progression and cell growth. In this study, we examined whether CRIF1 exerts an immunoregulatory effect by modulating the differentiation and function of pathogenic T cells. To this end, the role of CRIF1 in rheumatoid arthritis, a systemic autoimmune disease characterized by hyperplasia of synovial tissue and progressive destruction of articular cartilage structure by pathogenic immune cells [such as T helper type 17 (Th17) cells], was investigated. p3XFLAG-CMV-10-CRIF1 was administered to mice with collagen-induced arthritis 8 days after collagen type II immunization and the disease severity and histologic evaluation, and osteoclastogenesis were assessed. CRIF1 over-expression in mice with collagen-induced arthritis attenuated the clinical and histological signs of inflammatory arthritis. Furthermore, over-expression of CRIF1 in mice with arthritis significantly reduced the number of signal transducer and activator of transcription 3-mediated Th17 cells in the spleen as well as osteoclast differentiation from bone marrow cells. To investigate the impact of loss of CRIF1 in T cells, we generated a conditional CRIF1 gene ablation model using CD4-cre transgenic mice and examined the frequency of Th17 cells and regulatory T cells. Deficiency of CRIF1 in CD4
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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.