scholarly journals Interferon regulatory factor 3 as key element of the interferon signature in plasmacytoid dendritic cells from systemic lupus erythematosus patients: novel genetic associations in the Mexican mestizo population

2014 ◽  
Vol 178 (3) ◽  
pp. 428-437 ◽  
Author(s):  
K. Santana-de Anda ◽  
D. Gómez-Martín ◽  
A. E. Monsivais-Urenda ◽  
M. Salgado-Bustamante ◽  
R. González-Amaro ◽  
...  
Keyword(s):  
Systemic Lupus Erythematosus ◽  
Dendritic Cells ◽  
Lupus Erythematosus ◽  
Interferon Regulatory Factor ◽  
Genetic Associations ◽  
Regulatory Factor ◽  
Systemic Lupus ◽  
Interferon Signature ◽  
Mexican Mestizo ◽  
Mexican Mestizo Population

scholarly journals Interferon Regulatory Factor 5 in the Pathogenesis of Systemic Lupus Erythematosus

2012 ◽  
Vol 2012 ◽  
pp. 1-11 ◽  
Author(s):  
Candace M. Cham ◽  
Kichul Ko ◽  
Timothy B. Niewold
Keyword(s):  
Systemic Lupus Erythematosus ◽  
Lupus Erythematosus ◽  
Immune Complexes ◽  
Interferon Regulatory Factor ◽  
Immune Defense ◽  
Toll Like Receptors ◽  
Regulatory Factor ◽  
Systemic Lupus ◽  
Interferon Regulatory Factor 5

Systemic lupus erythematosus (SLE) is an autoimmune disease characterized by multiple genetic risk factors, high levels of interferon alpha (IFN-α), and the production of autoantibodies against components of the cell nucleus. Interferon regulatory factor 5 (IRF5) is a transcription factor which induces the transcription of IFN-αand other cytokines, and genetic variants of IRF5 have been strongly linked to SLE pathogenesis. IRF5 functions downstream of Toll-like receptors and other microbial pattern-recognition receptors, and immune complexes made up of SLE-associated autoantibodies seem to function as a chronic endogenous stimulus to this pathway. In this paper, we discuss the physiologic role of IRF5 in immune defense and the ways in whichIRF5variants may contribute to the pathogenesis of human SLE. Recent data regarding the role ofIRF5in both serologic autoimmunity and the overproduction of IFN-αin human SLE are summarized. These data support a model in which SLE-risk variants of IRF5 participate in a “feed-forward” mechanism, predisposing to SLE-associated autoantibody formation, and subsequently facilitating IFN-αproduction downstream of Toll-like receptors stimulated by immune complexes composed of these autoantibodies.

Association between the interferon regulatory factor 5 rs2004640 functional polymorphism and systemic lupus erythematosus: an updated meta-analysis

Lupus ◽  
2019 ◽  
Vol 28 (6) ◽  
pp. 740-747
Author(s):  
S C Bae ◽  
Y H Lee
Keyword(s):  
Systemic Lupus Erythematosus ◽  
Lupus Erythematosus ◽  
Meta Analysis ◽  
Asian Population ◽  
Interferon Regulatory Factor ◽  
European Population ◽  
Regulatory Factor ◽  
Systemic Lupus ◽  
Interferon Regulatory Factor 5 ◽  
Study Participants

Objective The aim of this study is to determine whether the functional interferon regulatory factor 5 ( IRF5) polymorphism rs2004640 is associated with susceptibility to systemic lupus erythematosus (SLE) in multiple ethnic populations. Methods A meta-analysis was conducted on the T allele of the IRF5 rs2004640 polymorphism in all study participants as well as each ethnic population. Results Twenty research articles that included 28 comparative studies of 20,892 patients and 24,930 controls were included in the meta-analysis. The Asian population had a much lower prevalence of the T allele than any other study population at 28%, and the European population had the highest prevalence of the T allele at 52%. Meta-analysis showed an association between the IRF5 rs2004640 polymorphism and SLE in all participants (odds ratio = 1.472, 95% confidence interval = 1.370–1.582, p < 0.001). Analysis after stratification by ethnicity indicated that the IRF5 rs2004640 T allele is significantly associated with SLE in Europeans, Asians, Latin Americans and Arabs. Conclusions This meta-analysis confirms that the IRF5 rs2004640 polymorphism is associated with SLE susceptibility in different ethnic groups, and that its prevalence is ethnicity dependent.

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