ArticleCommunications biology2022
Macrophage migration inhibitory factor is overproduced through EGR1 in TET2
Article in Communications biology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 26 citations in OpenAlex.
- TET2 loss enhances early response to inflammation in primitive and committed myeloid cells.Experimental hematology · 2026Article
- TET2 in epigenetic control of immune cells: Implications for inflammatory responses and age-related pathologies.The Journal of biological chemistry · 2026Review
- Metabolic control of innate immune activation in TET2-mutant clonal hematopoiesis.Cell chemical biology · 2026Article
- Crosstalk between metabolism and epigenetics during macrophage polarization.Epigenetics & chromatin · 2025Review
- Article
- Unravelling the role of TET2 in venous thromboembolism: insights into mechanisms and therapeutic implications.Frontiers in cardiovascular medicine · 2025Review
- RNA Shielding of p65 Is Required to Potentiate Oncogenic Inflammation in TET2-Mutated Clonal Hematopoiesis.Cancer discovery · 2024Article
- Targeting heterochromatin eliminates chronic myelomonocytic leukemia malignant stem cells through reactivation of retroelements and immune pathways.Communications biology · 2024Article
- CXCL8 secreted by immature granulocytes inhibits WT hematopoiesis in chronic myelomonocytic leukemia.The Journal of clinical investigation · 2024Article
- YTHDF2 favors protumoral macrophage polarization and implies poor survival outcomes in triple negative breast cancer.iScience · 2024Article
- Conditioned Medium Derived From Human Dental Follicle Mesenchymal Stem Cells Alleviates Macrophage Proinflammatory Responses Through MAPK-ERK-EGR1 Axis.Stem cells international · 2024Article
- SRSF2 plays an unexpected role as reader of mMolecular cell · 2023Article
- Clonal haematopoiesis and dysregulation of the immune system.Nature reviews. Immunology · 2023Review
Corrections and comments
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Authors and funding
20 authors at 6 institutions in 3 countries.
Funding
Abstract
Somatic mutation in TET2 gene is one of the most common clonal genetic events detected in age-related clonal hematopoiesis as well as in chronic myelomonocytic leukemia (CMML). In addition to being a pre-malignant state, TET2 mutated clones are associated with an increased risk of death from cardiovascular disease, which could involve cytokine/chemokine overproduction by monocytic cells. Here, we show in mice and in human cells that, in the absence of any inflammatory challenge, TET2 downregulation promotes the production of MIF (macrophage migration inhibitory factor), a pivotal mediator of atherosclerotic lesion formation. In healthy monocytes, TET2 is recruited to MIF promoter and interacts with the transcription factor EGR1 and histone deacetylases. Disruption of these interactions as a consequence of TET2-decreased expression favors EGR1-driven transcription of MIF gene and its secretion. MIF favors monocytic differentiation of myeloid progenitors. These results designate MIF as a chronically overproduced chemokine and a potential therapeutic target in patients with clonal TET2 downregulation in myeloid cells.
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