Polymorphisms in the gene encoding the transcription factor IRF5 that lead to higher mRNA expression are associated with many autoimmune diseases. Here we show that IRF5 expression in macrophages was reversibly induced by inflammatory stimuli and contributed to the plasticity of macrophage polarization. High expression of IRF5 was characteristic of M1 macrophages, in which it directly activated transcription of the genes encoding interleukin 12 subunit p40 (IL-12p40), IL-12p35 and IL-23p19 and repressed the gene encoding IL-10. Consequently, those macrophages set up the environment for a potent T helper type 1 (TH1)-TH17 response. Global gene expression analysis demonstrated that exogenous IRF5 upregulated or downregulated expression of established phenotypic markers of M1 or M2 macrophages, respectively. Our data suggest a critical role for IRF5 in M1 macrophage polarization and define a previously unknown function for IRF5 as a transcriptional repressor.

Irf5 promotes inflammatory macrophage polarization and th1/th17 response

MicroRNAs (miRNAs) are endogenous ∼23 nt RNAs that play important gene-regulatory roles in animals and plants by pairing to the mRNAs of protein-coding genes to direct their posttranscriptional repression. This review outlines the current understanding of miRNA target recognition in animals and discusses the widespread impact of miRNAs on both the expression and evolution of protein-coding genes.

MicroRNAs: Target Recognition and Regulatory Functions

Macrophage polarization and allergic asthma

The Interferon regulatory factors (IRFs) are a family of transcription factors that play pivotal roles in many aspects of the immune response, including immune cell development and differentiation and regulating responses to pathogens. Three family members, IRF3, IRF5, and IRF7, are critical to production of type I interferons downstream of pathogen recognition receptors that detect viral RNA and DNA. A fourth family member, IRF9, regulates interferon-driven gene expression. In addition, IRF4, IRF8, and IRF5 regulate myeloid cell development and phenotype, thus playing important roles in regulating inflammatory responses. Thus, understanding how their levels and activity is regulated is of critical importance given that perturbations in either can result in dysregulated immune responses and potential autoimmune disease. This review will focus the role of IRF family members in regulating type I IFN production and responses and myeloid cell development or differentiation, with particular emphasis on how regulation of their levels and activity by ubiquitination and microRNAs may impact autoimmune disease.

/pdf/regulating-irfs-in-ifn-driven-disease-xynjp3l96n.pdf

Regulating IRFs in IFN Driven Disease.

MicroRNAs (miRNAs or miRs) are a class of evolutionarily-conserved small, regulatory non-coding RNAs, 19–3 nucleotides in length, that negatively regulate protein coding gene transcripts’ expression. miR-146 (146a and 146b) and miR-155 are among the first and most studied miRs for their multiple roles in the control of the innate and adaptive immune processes and for their deregulation and oncogenic role in some tumors. In the present review, we have focused on the recent acquisitions about the key role played by miR-146a, miR-146b and miR-155 in the control of the immune system and in myeloid tumorigenesis. Growing experimental evidence indicates an opposite role of miR-146a with respect to miR-155 in the fine regulation of many steps of the immune response, acting at the level of the various cell types involved in innate and adaptive immune mechanisms. The demonstration that miR-155 overexpression plays a key pathogenic role in some lymphomas and acute myeloid leukemias has led to the development of an antagomir-based approach as a new promising therapeutic strategy.

miR-146 and miR-155: Two Key Modulators of Immune Response and Tumor Development.

Reprogramming macrophage orientation by microRNA 146b targeting transcription factor IRF5

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Reprogramming macrophage orientation by microRNA 146b targeting transcription factor IRF5