Interferon regulatory factor 5 (IRF5) has been demonstrated as a key transcription
factor of the immune system, playing important roles in modulating inflammatory immune
responses in numerous cell types including dendritic cells, macrophages, and B cells.
As well as driving the expression of type I interferon in antiviral responses, IRF5
is also crucial for driving macrophages toward a proinflammatory phenotype by regulating
cytokine and chemokine expression and modulating B-cell maturity and antibody production.
This review highlights the functional importance of IRF5 in a disease setting, by
discussing polymorphic mutations at the human Irf5 locus that lead to susceptibility to systemic lupus erythematosus, rheumatoid arthritis,
and inflammatory bowel disease. In concordance with this, we also discuss lessons
in IRF5 functionality learned from murine in vivo models of autoimmune disease and
inflammation and hypothesize that modulation of IRF5 activity and expression could
provide potential therapeutic benefits in the clinic.
Abbreviations:
GWAS (genome wide association study), IBD (inflammatory bowel disease), IFN (interferon), IRF (interferon regulatory factor), RA (rheumatoid arthritis), SLE (systemic lupus erythematosus), SNP (single nucleotide polymorphism)To read this article in full you will need to make a payment
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Article info
Publication history
Published online: July 03, 2015
Accepted:
June 30,
2015
Received in revised form:
June 29,
2015
Received:
April 15,
2015
Identification
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© 2016 Elsevier Inc. Published by Elsevier Inc. All rights reserved.
