IRF5 Rôles | Notes et références | Menu de navigationIRF5 promotes inflammatory macrophage polarization and TH1-TH17 responsesIrf5 deficiency in macrophages promotes beneficial adipose tissue expansion and insulin sensitivity during obesityIn vivo silencing of the transcription factor IRF5 reprograms the macrophage phenotype and improves infarct healingInterferon Regulatory Factor 5 controls necrotic core formation in atherosclerotic lesions by impairing efferocytosis

Facteur de transcriptionChromosome 7 humain


facteurs de régulation de l'interféronfacteur de transcriptionChromosome 7 humaininterleukines 1223interleukine 10résistance à l'insulineinfarctus du myocardeathéromeefférocytose




L'IRF (pour « Interferon regulatory factor 5 ») est une protéine de la famille des facteurs de régulation de l'interféron, avec un rôle de facteur de transcription. Son gène est IRF5 situé sur le Chromosome 7 humain.



Rôles |


il augmente l'expression des sous-unités es interleukines 12 et 23 et diminue celle de l'interleukine 10[1].


Il favorise la résistance à l'insuline et modifie la répartition des graisses[2].


Son inhibition pourrait améliorer la cicatrisation cardiaque après un infarctus du myocarde[3].


Dans l'athérome, il aurait un rôle pro-inflammatoire et inhiberait l'efférocytose[4].



Notes et références |



  1. Krausgruber T, Blazek K, Smallie T et al. IRF5 promotes inflammatory macrophage polarization and TH1-TH17 responses, Nat Immunol, 2011;12:231–238


  2. Dalmas E, Toubal A, Alzaid F et al. Irf5 deficiency in macrophages promotes beneficial adipose tissue expansion and insulin sensitivity during obesity, Nat Med, 2015;21:610–618


  3. Courties G, Heidt T, Sebas M et al. In vivo silencing of the transcription factor IRF5 reprograms the macrophage phenotype and improves infarct healing, J Am Coll Cardiol, 2014;63:1556–1566


  4. Seneviratne AN, Edsfeldt A, Cole JE et al. Interferon Regulatory Factor 5 controls necrotic core formation in atherosclerotic lesions by impairing efferocytosis, Circulation, 2017;136:1140-1154


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