ArticleClinical & developmental immunology2011
IFN regulatory factors 4 and 8 expression in the NOD mouse.
Article in Clinical & developmental immunology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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
5 citing papers in PubMed, 8 citations in OpenAlex.
- Oral exposure to PET microplastics induces the pancreatic immune response and oxidative stress in immature pigs.BMC genomics · 2025Article
- Integrative analyses of biomarkers and pathways for diabetic nephropathy.Frontiers in genetics · 2023Article
- Dendritic Cells and Their Immunotherapeutic Potential for Treating Type 1 Diabetes.International journal of molecular sciences · 2022Review
- Bioinformatics Analysis of the Mechanisms of Diabetic NephropathyFrontiers in endocrinology · 2022Article
- Collagen I-induced dendritic cells activation is regulated by TNF-alpha production through down-regulation of IRF4.Journal of biosciences · 2015Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Dendritic cells (DCs) contribute to islet inflammation and its progression to diabetes in NOD mouse model and human. DCs play a crucial role in the presentation of autoantigen and activation of diabetogenic T cells, and IRF4 and IRF8 are crucial genes involved in the development of DCs. We have therefore investigated the expression of these genes in splenic DCs during diabetes progression in NOD mice. We found that IRF4 expression was upregulated in splenocytes and in splenic CD11c(+) DCs of NOD mice as compared to BALB/c mice. In contrast, IRF8 gene expression was higher in splenocytes of NOD mice whereas its expression was similar in splenic CD11c(+) DCs of NOD and BALB/c mice. Importantly, levels of IRF4 and IRF8 expression were lower in tolerogenic bone marrow derived DCs (BMDCs) generated with GM-CSF as compared to immunogenic BMDCs generated with GM-CSF and IL-4. Analysis of splenic DCs subsets indicated that high expression of IRF4 was associated with increased levels of CD4(+)CD8α(-)IRF4(+)CD11c(+) DCs but not CD4(-)CD8α(+)IRF8(+)CD11c(+) DCs in NOD mice. Our results showed that IRF4 expression was up-regulated in NOD mice and correlated with the increased levels of CD4(+)CD8α(-) DCs, suggesting that IRF4 may be involved in abnormal DC functions in type 1 diabetes in NOD mice.
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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.