Interferon regulatory factor 5 in human autoimmunity and murine models of autoimmune disease

Eames, Hayley L.; Corbin, Alastair; Udalova, Irina A.

doi:10.1016/j.trsl.2015.06.018

Cited by 67 publications

(68 citation statements)

References 165 publications

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“…IRF5 expression can be enhanced by a positive feedback loop. In inflammatory conditions, IRF5 stimulation promoted IFN‐α generation via Toll‐like receptors (TLRs), while evaluated IFN‐α production may positively up‐regulate the expression of IRF5 . Studies in mice models suggest the important role for IRF5 in SLE, by which mice lacking the IRF5 gene failed to promote the TLR‐mediated pro‐inflammatory cytokines production .…”

Section: Discussionmentioning

confidence: 99%

Association of IRF5 rs2004640 polymorphism and systemic lupus erythematosus: A meta‐analysis

et al. 2019

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Background This study aimed to discuss the relationship between interferon regulatory factor (IRF)5 gene rs2004640 T/G polymorphism and systemic lupus erythematosus (SLE) susceptibility. Methods A meta‐analysis was calculated on the association between rs2004640 polymorphism and SLE by allelic contrast (T vs G), additive model (TT vs GG), recessive model (TT vs TG + GG) and dominant model (TT + TG vs GG). Results A total of 28 comparisons were identified, including 11 228 SLE cases and 14 374 controls. Meta‐analysis revealed a significant association between allele T and SLE in overall populations (odds ratio [OR] = 1.393, 95% CI: 1.276‐1.522, P < 0.001). Stratification by ethnicity indicated strong associations between T allele and SLE in Asians, Europeans and Latin Americans (OR = 1.256, 95% CI: 1.073‐1.469, P = 0.004; OR = 1.338, 95% CI: 1.080‐1.659, P = 0.008; OR = 1.853, 95% CI: 1.488‐2.308, P < 0.001). Results also showed significant associations between the additive model and SLE in all subjects and Asians (OR = 1.999, 95% CI: 1.442‐2.771, P < 0.001; OR = 1.544, 95% CI: 1.009‐2.362, P < 0.045). In addition, we found significant associations between the dominant model and SLE in all populations and Asians (OR = 1.521, 95% CI: 1.257‐1.841, P < 0.001; OR = 1.270, 95% CI: 1.136‐1.421, P < 0.001). A marginal association was detected between the recessive mode and SLE in overall subjects (OR = 1.480, 95% CI: 1.022‐2.144, P = 0.038). Conclusion The current study suggested that individuals carrying rs2004640 T allele correlated with a high risk of SLE, and the IRF5 rs2004640 polymorphism was associated with SLE susceptibility.

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Section: Discussionmentioning

confidence: 99%

Association of IRF5 rs2004640 polymorphism and systemic lupus erythematosus: A meta‐analysis

et al. 2019

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“…Contributions of the NLRP3 inflammasome to inflammatory disorders are also described. Signaling pathways in human autoimmune diseases as well as in mouse autoimmune diseases have been delineated (47). Vaccination of patients who are afflicted with autoimmune diseases, using clinically safe and effective vaccines, may lead to protective outcomes (48).…”

Section: The Nlrp3 Inflammasomementioning

confidence: 99%

Anti-inflammatory interventions—what has worked, not worked, and what may work in the future

Fattahi

Ward

2016

Translational Research

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Our Introductory Commentary relates to many topics that are linked to inflammatory responses and how these responses are regulated in order to promote healing of damaged tissues and bring about effective clearance of infectious agents. In non-infectious situations, cells and tissues release products (danger associated molecular patterns) that can trigger damaging inflammatory responses. These products must be effectively dealt with in order to avoid serious tissue injury. We provide a perspective about many decades of research into the inflammatory response and describe strategies that have achieved success in restraining inflammatory responses, as well as many approaches that have not been clinically effective. With development of new technologies such as advanced genomic analysis, highly sensitive and sophisticated mass spectrometry and related approaches, as well as the ability to employ mutagenesis induction, we are beginning to define highly sophisticated molecular pathways that previously were opaque. This progress may well have clinical relevance, and we may be on the edge of a scientific revolution in the broad area of inflammation.

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“…With the success in genetic discoveries, an important challenge has been to define the mechanisms through which identified genes contribute to disease pathogenesis. The transcription factor IFN regulatory factor 5 (IRF5) is one such gene identified as an autoimmune susceptibility gene (10). IRF5 is a critical downstream mediator of MyD88-dependent Toll-like receptor (TLR) signaling that regulates both arms of the immune system -innate and adaptive (10)(11)(12)(13).…”

Section: Introductionmentioning

confidence: 99%

IRF5 genetic risk variants drive myeloid-specific IRF5 hyperactivation and presymptomatic SLE

Matta

et al. 2020

JCI Insight

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Interferon regulatory factor 5 in human autoimmunity and murine models of autoimmune disease

Cited by 67 publications

References 165 publications

Association of IRF5 rs2004640 polymorphism and systemic lupus erythematosus: A meta‐analysis

Association of IRF5 rs2004640 polymorphism and systemic lupus erythematosus: A meta‐analysis

Anti-inflammatory interventions—what has worked, not worked, and what may work in the future

IRF5 genetic risk variants drive myeloid-specific IRF5 hyperactivation and presymptomatic SLE

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