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Sjögren Syndrome
Published in Dongyou Liu, Handbook of Tumor Syndromes, 2020
The IRF5 (interferon regulatory factor 5) gene encodes a transcription factor that mediates type I interferon responses in monocytes, dendritic cells, and B cells upon viral infection, leading to the transcription of interferon-α genes and the production of proinflammatory cytokines (e.g., IL-12, p40, IL-6, and TNFα). IRF5 (possibly in association with the neighboring gene TNPO3 s) represents an established risk locus in systemic lupus erythematosus (SLE), rheumatoid arthritis, ulcerative colitis, primary biliary cirrhosis, and systemic sclerosis (SSc). Among known IRF5 pathogenic variants, a CGGGG indel polymorphism in the promoter region is strongly linked to Sjögren syndrome [5].
Human Herpesvirus Type 8/Kaposi Sarcoma Herpesvirus
Published in Satya Prakash Gupta, Cancer-Causing Viruses and Their Inhibitors, 2014
Hiba El Hajj, Raghida Abou Merhi, Ali Bazarbachi
Another latent protein, LANA-2, also known as viral interferon regulatory factor 3 (vIRF3), is expressed in the nuclei of virtually all HHV-8-infected lymphoid cells in primary effusion lymphoma (PEL) and in the majority of HHV-8-infected cells in multicentric Castleman’s disease (MCD) but not in KS (Cunningham et al. 2003). LANA-2 is expressed during latency and antagonizes p53-mediated apoptosis in vitro (Wies et al. 2008). It stimulates c-Myc function (Lubyova et al. 2007) and stabilizes HIF-1α and pro-apoptotic cellular interferon regulatory factor-5 (IRF-5) (Shin et al. 2008). It was shown that it stimulates growth inhibition via G2/M cell cycle arrest (Table 10.2) (Bi et al. 2011). LANA-2 was also shown to directly interact with cellular IRF-3, IRF-7, and the transcriptional co-activator CBP/p300, and to stimulate their transcriptional activity, leading to enhanced expression of type I interferon and chemokine genes (Lubyova et al. 2004).
Precision medicine in multiple sclerosis
Published in Debmalya Barh, Precision Medicine in Cancers and Non-Communicable Diseases, 2018
Differences in ethnicity also have the potential to affect the pharmacokinetic profile of the drugs (Wu et al., 2012). Interferon regulatory factor 5 (IRF5) gene can affect IFNβ therapy in MS (Vandenbroeck et al., 2011). IRF5 variants affect clinical outcomes of IFNβ therapy (Vosslamber et al., 2011). Pharmacogenomic analysis of response to IFNβ therapy in MS has been reported (Byun et al., 2008). Anti-John Cunningham (anti-JC) virus antibodies are utilized in the safety monitoring of natalizumab therapy (Bloomgren et al., 2012). Several biomarkers have been identified for MS treatment (Derfuss, 2012) and are classified as follows: Established biomarkers (with valid evidence) Neutralizing antibodies against natalizumabAntibodies against JC virusEstablished biomarkers (with some experimental/clinical evidence) Magnetic resonance imagingNeutralizing antibodies against beta-interferonAquaporin 4 antibodiesPotential biomarkers (with some experimental/clinical evidence) CD56 bright natural killer cellsCytokines/chemokinesTranscriptomicsGenetics
IRF5-mediated immune responses and its implications in immunological disorders
Published in International Reviews of Immunology, 2018
Ashwinder Kaur, Learn-Han Lee, Sek-Chuen Chow, Chee-Mun Fang
IRF5 is constitutively expressed in lymphoid tissues such as spleen and peripheral blood lymphocytes.13 In the latter, the expression of IRF5 is mainly found in B cells and barely in T cells and natural killer (NK) cells. Higher level of IRF5 expression has been found in other immune cells such as monocytes and macrophages but relatively lower in dendritic cells.20,21 Other factors such as viral infection and IFNα stimulation could enhance the expression of IRF5.20,22 Notably, the expression of IRF5 is found to be either absent or down-regulated in most cancer cell lines.21 This indicates the inclination of IRF5 for gene deletion or epigenetic silencing in these malignancies.17,23,24 The importance of IRF5 in regulating immune cells functions and its expression dysregulation in the pathogenesis of immune system disorders is summarized in Table 1.