ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2010
Genetic deficiency of Irgm1 (LRG-47) suppresses induction of experimental autoimmune encephalomyelitis by promoting apoptosis of activated CD4+ T cells.
Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 34 citations in OpenAlex.
- IRGM Deficiency Exacerbates Sepsis-Induced Acute Lung Injury by Inhibiting Autophagy Through the AKT/mTOR Signaling Pathway.Journal of inflammation research · 2024Article
- Research progress of T cell autophagy in autoimmune diseases.Frontiers in immunology · 2024Review
- Diagnostic Potential of Two Novel Biomarkers for Neuromyelitis Optica Spectrum Disorder and Multiple Sclerosis.Diagnostics (Basel, Switzerland) · 2023Article
- How did we get here? Insights into mechanisms of immunity-related GTPase targeting to intracellular pathogens.Current opinion in microbiology · 2022Review
- Dendritic cell PIK3C3/VPS34 controls the pathogenicity of CNS autoimmunity independently of LC3-associated phagocytosis.Autophagy · 2022Article
- Pharmacological insights into autophagy modulation in autoimmune diseases.Acta pharmaceutica Sinica. B · 2021Review
- Relevance of Autophagy and Mitophagy Dynamics and Markers in Neurodegenerative Diseases.Biomedicines · 2021Review
- Autoimmunity gene IRGM suppresses cGAS-STING and RIG-I-MAVS signaling to control interferon response.EMBO reports · 2020Article
- Regulation of hippocampal neuronal apoptosis and autophagy in mice with sepsis-associated encephalopathy by immunity-related GTPase M1.CNS neuroscience & therapeutics · 2020Article
- Irgm1 coordinately regulates autoimmunity and host defense at select mucosal surfaces.JCI insight · 2017Article
- Article
- IFNAR signaling directly modulates T lymphocyte activity, resulting in milder experimental autoimmune encephalomyelitis development.Journal of leukocyte biology · 2016Article
- Review
- IFNg-induced Irgm1 promotes tumorigenesis of melanoma via dual regulation of apoptosis and Bif-1-dependent autophagy.Oncogene · 2015Article
- Role of autophagy in the pathogenesis of multiple sclerosis.Neuroscience bulletin · 2015Article
- IRGM1 enhances B16 melanoma cell metastasis through PI3K-Rac1 mediated epithelial mesenchymal transition.Scientific reports · 2015Article
- Article
- Temporal gene profiling of the 5XFAD transgenic mouse model highlights the importance of microglial activation in Alzheimer's disease.Molecular neurodegeneration · 2014Article
- Irgm1 (LRG-47), a regulator of cell-autonomous immunity, does not localize to mycobacterial or listerial phagosomes in IFN-γ-induced mouse cells.Journal of immunology (Baltimore, Md. : 1950) · 2013Article
- Quantitative proteomics for identifying biomarkers for Rabies.Clinical proteomics · 2013Article
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Authors and funding
10 authors at 5 institutions in 1 country.
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Abstract
The immunity-related GTPase Irgm1, also called LRG-47, is known to regulate host resistance to intracellular pathogens through multiple mechanisms that include controlling the survival of T lymphocytes. Here, we address whether Irgm1 also plays a role in the pathogenesis of experimental autoimmune encephalitis (EAE). We find that Irgm1/LRG-47 is a significant factor in the progression of EAE and multiple sclerosis (MS). Expression of Irgm1 was robustly elevated in MS-affected lesions and in the central nervous system (CNS) of myelin basic protein (MBP)-induced EAE mice, especially in cells of lymphoid and mononuclear phagocyte origin. Homozygous Irgm1 null mice were resistant to MBP-induced EAE, and CD4(+) T cells in spleen and CNS of these mice displayed decreased proliferative capacity, increased apoptosis, and up-regulated interferon (IFN)-gamma induction. Therefore, Irgm1-induced survival of autoreactive CD4(+) T cells contributes significantly to the pathogenesis of EAE. Blockade of Irgm1 may be a potential therapeutic strategy for halting multiple sclerosis.
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