scholarly journals Interferon regulatory factor 5 (IRF5) gene variants are associated with multiple sclerosis in three distinct populations

2008 ◽  
Vol 45 (6) ◽  
pp. 362-369 ◽  
Author(s):  
G Kristjansdottir ◽  
J K Sandling ◽  
A Bonetti ◽  
I M Roos ◽  
L Milani ◽  
...  
2012 ◽  
Vol 13 (5) ◽  
pp. 443-443 ◽  
Author(s):  
S Vosslamber ◽  
L F van der Voort ◽  
I J van den Elskamp ◽  
R Heijmans ◽  
C Aubin ◽  
...  

2011 ◽  
Vol 12 (6) ◽  
pp. 466-472 ◽  
Author(s):  
S Vosslamber ◽  
L F van der Voort ◽  
I J van den Elskamp ◽  
R Heijmans ◽  
C Aubin ◽  
...  

2011 ◽  
Vol 38 (10) ◽  
pp. 2130-2132 ◽  
Author(s):  
CHUAN WANG ◽  
HEIDI KOKKONEN ◽  
JOHANNA K. SANDLING ◽  
MARTIN JOHANSSON ◽  
MARIA SEDDIGHZADEH ◽  
...  

Objective.Two interferon regulatory factor 5 (IRF5) gene variants were examined for association with rheumatoid arthritis (RA).Methods.A total of 2300 patients with RA and 1836 controls were recruited from 2 independent RA studies in Sweden. One insertion-deletion polymorphism (CGGGG indel) and one single-nucleotide polymorphism (rs10488631) in the IRF5 gene were genotyped and analyzed within RA subgroups stratified by rheumatoid factor (RF) and anticitrullinated peptide antibodies (ACPA).Results.The CGGGG indel was preferentially associated with the RF-negative (OR 1.29, p = 7.9 × 10−5) and ACPA-negative (OR 1.27, p = 7.3 × 10−5) RA subgroups compared to the seropositive counterparts. rs10488631 was exclusively associated within the seronegative RA subgroups (RF-negative: OR 1.24, p = 0.016; ACPA-negative: OR 1.27, p = 4.1 × 10−3).Conclusion.Both the CGGGG indel and rs10488631 are relevant for RA susceptibility, especially for seronegative RA.


2014 ◽  
Vol 21 (8) ◽  
pp. 984-995 ◽  
Author(s):  
Davide Cossu ◽  
Giuseppe Mameli ◽  
Grazia Galleri ◽  
Eleonora Cocco ◽  
Speranza Masala ◽  
...  

Background: A large number of reports indicate the association of Epstein-Barr virus (EBV), and Mycobacterium avium subsp. paratuberculosis (MAP) with multiple sclerosis (MS). Objective: To gain a better understanding of the role of these two pathogens, we investigated the host response induced by selected antigenic peptides. Methods: We examined both humoral and cell-mediated responses against peptides deriving from EBV tegument protein BOLF1, the MAP_4027 and the human interferon regulatory factor 5 (IRF5424–434) homolog in several MS patients and healthy controls (HCs). Results: Antibodies against these peptides were highly prevalent in MS patients compared to HCs. Concerning MS patients, BOLF1305–320, MAP_402718–32 and IRF5424–434 peptides were able to induce mainly Th1-related cytokines secretion, whereas Th2-related cytokines were down-regulated. Flow cytometry analyses performed on a subset of MS patients highlighted that these peptides were capable of inducing the release of pro-inflammatory cytokines: IFN-γ and TNF-α by CD4+ and CD8+ T lymphocytes, and IL-6 and TNF-α by CD14+ monocyte cells. Conclusion: Our data demonstrated that both EBV and MAP epitopes elicit a consistent humoral response in MS patients compared to HCs, and that the aforementioned peptides are able to induce a T-cell-mediated response that is MS correlated.


2007 ◽  
Vol 56 (7) ◽  
pp. 2202-2210 ◽  
Author(s):  
Snaevar Sigurdsson ◽  
Leonid Padyukov ◽  
Fina A. S. Kurreeman ◽  
Ulrika Liljedahl ◽  
Ann-Christin Wiman ◽  
...  

2012 ◽  
Vol 40 (2) ◽  
pp. 1791-1799 ◽  
Author(s):  
Young Ho Lee ◽  
Sang-Cheol Bae ◽  
Sung Jae Choi ◽  
Jong Dae Ji ◽  
Gwan Gyu Song

2020 ◽  
Vol 11 ◽  
Author(s):  
Ziqi Fan ◽  
Shuai Zhao ◽  
Yueli Zhu ◽  
Zheyu Li ◽  
Zhirong Liu ◽  
...  

BackgroundActivated microglia play a vital role in neuroinflammation in the central nervous system (CNS), which is associated with the pathogenesis and the progression of neurological diseases. Interferon regulatory factor 5 (IRF5) has been well established participating in inflammatory responses and is highly expressed in M1 macrophage in the periphery, the role of which in the CNS remains elusive.MethodsLipopolysaccharide (LPS) was employed to induce neuroinflammation. Down-regulation of IRF5 in C57/BL6 mice and BV2 microglial cells were achieved by IRF5 siRNA transfection. The levels of pro-inflammatory cytokines were evaluated by ELISA and quantitative real-time PCR. The expression levels of IRF5 were examined by immunofluorescence and Western blot.ResultsLPS induced significantly elevated expression of IRF5 in mouse brain, which co-localized with CD11b-positive microglia. Down-regulation of IRF5 quenched the pro-inflammatory responses. The levels of pro-inflammatory cytokines TNF-α, IL-1β, and IL-6 were up-regulated at 4 h after LPS treatment, which were significantly down-regulated with the knockdown of IRF5. LPS-induced pro-inflammatory responses were transient, which were comparable to control group at 24 h after LPS treatment. However, LPS did not up-regulate the expression of IRF5 in BV2 microglial cells, indicating that LPS-induced inflammation in BV2 cells does not involve IRF5 signaling.ConclusionsIRF5 mediates the inflammatory responses in the CNS, which might serve as a therapeutic target for CNS inflammatory diseases. LPS-induced inflammation does not involve IRF5 signaling in BV2 microglia.


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