IRF5


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IRF5

A gene on chromosome 7q32 that encodes a member of the interferon regulatory transcription factor (IRF) family, which have diverse roles such virus-mediated activation of interferons and modulation of cell growth, differentiation, apoptosis and immune system activity.
References in periodicals archive ?
IRF8 binds directly to the promoter loci of IRF5 and activates the transcription of IRF5, resulting in the increase of IRF5.
In addition, boosting IRF5 levels might help to treat people whose immune systems are compromised.
Two high-density (43,44) and one low-density GWAS45 in SLE have recently been published, yielding definitive data about several new risk genes, as well as valuable confirmatory data related to several previously identified genes, including STAT4 and IRF5. Although results of GWAS in SLE and other human autoimmune diseases have significantly advanced our understanding of the genetic contribution to these diseases, it is also clear that even larger sample sizes and denser or different genetic marker sets will be required to allow us to fully benefit from this new and exciting methodology.
The transcription factor IRF5 is another major regulator of proinflammatory M1 macrophage polarization.
A functionally relevant IRF5 haplotype is associated with reduced risk to Wegener's granulomatosis.
Blocking the production of IRF5 could help in a range of diseases including RA, lupus and even MS.
Otros genes candidatos con fuerte evidencia han sido identificados mediante GWAS incluyendo IRF5, BLK, y STAT4.
Recently, a genetic cohort study was conducted to evaluate new regions associated with SS, showing a correlation with the (major histocompatibility complex) MHC region and the presence of innate immune system pathway activation, the interferon regulatory factor 5 (IRF5), T cell activation (HLA and MHC associations, STAT4, IL12, KLRG1, SH2D2A, and NFAT5), and NF-[kappa]B activation (TNIP1 and TNFAIP3) [24, 25].
Honda, "Contribution of IRF5 in B cells to the development of murine SLE-like disease through its transcriptional control of the IgG2a locus," Proceedings of the National Acadamy of Sciences of the United States of America, vol.
Recently it has been published that TRAF-2 controls the fate of IRF5 and c-Rel by proteasomal degradation via TRAF3 and cIAP.
Several DEGs involved in the innate immune response (i.e., HDX9, DDX3X, SOCS3, STAT1, IRF5, IFIT2, and STAT2) were present in clusters CL2 and CL3.
Yoshinaga et al., "Transcription factor IRF5 drives P2X4R+-reactive microglia gating neuropathic pain," Nature Communications, vol.