Regular ArticlesComplete Suppression of Insulitis and Diabetes in NOD mice Lacking Interferon Regulatory Factor-1
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Immune regulator IRF1 contributes to ZBP1-, AIM2-, RIPK1-, and NLRP12-PANoptosome activation and inflammatory cell death (PANoptosis)
2023, Journal of Biological ChemistryThe interferon regulatory factors, a double-edged sword, in the pathogenesis of type 1 diabetes
2022, Cellular ImmunologyCitation Excerpt :IRF1 has been suggested as a T1D risk gene and a well-identified pro-apoptotic tumor suppressor in malignant diseases [35,36]. The non-obese diabetic (NOD) mice deficient in Irf1 do not develop diabetes along with the decrease of CD8 T and B cell proportions in the spleen [37]. IRF1 plays a pivotal part in mediating the cytotoxic effect of TNF-α, IFN-γ and IL-1β, which are mostly appreciated for causing β cell destruction.
SARS-CoV-2 infection impairs the insulin/IGF signaling pathway in the lung, liver, adipose tissue, and pancreatic cells via IRF1
2022, Metabolism: Clinical and ExperimentalGenes and transcription factors related to the adverse effects of maternal type I diabetes mellitus on fetal development
2019, Molecular and Cellular ProbesCitation Excerpt :Single nucleotide polymorphisms rs1711968 and rs732835 in FOXF2 are associated with non-syndromic cleft lip [49]. Autoimmune diabetes is completely suppressed in IRF1-deficient non-obese diabetic mice [50], and IRF1 plays a crucial role in preterm labor [51]. Non-coding mutations in OVOL2 promoter can cause autosomal-dominant corneal endothelial dystrophies [52].
Interferon alpha: The key trigger of type 1 diabetes
2018, Journal of AutoimmunityCitation Excerpt :Elevated levels of pDCs, which are key producers of IFNα, were also reported in pancreatic draining lymph nodes of young (2–3 weeks old) NOD mice, supporting the notion that local IFNα produced by pDCs plays a critical role in T1D etiology [47]. The relationship between IFNα and T1D in NOD mice was also confirmed in mice lacking the interferon regulatory factor-1 (IRF-1−/− NOD mice) in which the development of insulitis and diabetes was completely suppressed [48]. Additional support for the role of IFNα in triggering T1D came from studies in BB rats (that spontaneously develop T1D) [49] and in low dose streptozotocin-treated mice that also develop a T1D-like disease [42].
Interferon regulatory factor signaling in autoimmune disease
2017, CytokineCitation Excerpt :Non-obese diabetic (NOD) mice are a widely used animal model of autoimmune diabetes. Nakazawa et al. bred Irf1−/− C57BL/6J mice onto the NOD background to examine its role in autoimmune diabetes development [152]. Loss of Irf1 completely blocked the development of insulitis and diabetes.
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Correspondence to: Dr Jo Satoh, Division of Molecular Metabolism and Diabetes, Department of Internal Medicine, Tohoku University School of Medicine, 1-1 Seiryo-machi, Aoba-ku, Sendai, 980-8574, Japan. Fax +81-22-717-7177. E-mail:[email protected]