Influence of TRAF1/C5 and STAT4 genes polymorphisms on susceptibility and severity of rheumatoid arthritis in Egyptian population

Mohamed, Rasha H.; Pasha, Heba F.; El-Shahawy, Eman E.

doi:10.1016/j.cellimm.2011.11.005

Cited by 29 publications

(20 citation statements)

References 35 publications

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“…Given the roles of C5 in chronic inflammation, such as hepatitis B-induced liver fibrosis (52), and in the pathogenesis of cerebral and placental malaria (53), we propose that the complement system also plays a significant role in C. trachomatis induction of hydrosalpinx in women. This hypothesis is consistent with the finding of significant association of the TRAF1/C5 A allele with rheumatoid arthritis (57). Nevertheless, we should be cautious in interpreting the data from the C. muridarum murine genital tract infection model, because it has been recently shown that genital tract infection with C. trachomatis in mice can be controlled by innate immunity alone, while adaptive immunity is required to control C. muridarum genital tract infection (58), highlighting the difference in invasiveness between C. trachomatis and C. muridarum.…”

Section: Muridarum (A) Mice Without (C5supporting

confidence: 92%

Complement Factor C5 but Not C3 Contributes Significantly to Hydrosalpinx Development in Mice Infected with Chlamydia muridarum

et al. 2014

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bHydrosalpinx is a pathological hallmark of tubal infertility associated with chlamydial infection. However, the mechanisms of hydrosalpinx remain unknown. Here, we report that complement factor 5 (C5) contributes significantly to chlamydial induction of hydrosalpinx. Mice lacking C5 (C5 ؊/؊ ) failed to develop any hydrosalpinx, while ϳ42% of the corresponding wild-type mice (C5 ؉/؉ ) did so following intravaginal infection with Chlamydia muridarum. Surprisingly, deficiency in C3 (C3 ؊/؊ ), an upstream component of the complement system, did not affect mouse susceptibility to chlamydial induction of hydrosalpinx. Interestingly, C5 activation was induced by chlamydial infection in oviducts of C3 ؊/؊ mice, explaining why the C3 ؊/؊ mice remained susceptible to chlamydial induction of hydrosalpinx. Similar levels of live chlamydial organisms were recovered from oviduct tissues of both C5 ؊/؊ and C5 ؉/؉ mice, suggesting that C5 deficiency did not affect C. muridarum ascending infection. Furthermore, C5؊/؊ mice were still more resistant to hydrosalpinx induction than C5 ؉/؉ mice, even when live C. muridarum organisms were directly delivered into the upper genital tract, both confirming the role of C5 in promoting hydrosalpinx and indicating that the C5-facilitated hydrosalpinx was not due to enhancement of ascending infection. The C5 ؊/؊ mice displayed significantly reduced lumenal inflammatory infiltration and cytokine production in oviduct tissue, suggesting that C5 may contribute to chlamydial induction of hydrosalpinx by enhancing inflammatory responses.

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Section: Muridarum (A) Mice Without (C5supporting

confidence: 92%

Complement Factor C5 but Not C3 Contributes Significantly to Hydrosalpinx Development in Mice Infected with Chlamydia muridarum

et al. 2014

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“…RA susceptibility variants mapping to the TRAF1/C5 locus on chromosome 9 have previously been investigated for association with radiological outcome in patients with RA 1,13,14,15 . Based on recent evidence, it seems that the originally reported LD block containing rs3761847, rs10818488, and rs10760130 is not associated with radiological severity across several populations 14 .…”

Section: Discussionmentioning

confidence: 99%

“…A recent study replicated the association of rs3761847 with radiological damage in Iceland, but could not replicate this association or the association of rs10818488 in 6 other cohorts originating from different countries 14 . Another recent study showed rs10818488 to be associated with radiological damage in Egyptian patients 15 . However, there have been no published reports investigating rs2900180 in an independent population.…”

mentioning

confidence: 97%

Investigation of Rheumatoid Arthritis Genetic Susceptibility Markers in the Early Rheumatoid Arthritis Study Further Replicates the TRAF1 Association with Radiological Damage

Plant¹,

Fu²,

Flynn³

et al. 2012

J Rheumatol

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Objective.The TRAF1 genetic region conferring susceptibility to rheumatoid arthritis (RA) has been reported to associate with radiological damage. We aimed to test RA genetic susceptibility markers for association with a continuous measure of radiological damage over time using longitudinal modeling techniques.Methods.Sixty-seven RA susceptibility variants were genotyped in 474 patients in the Early Rheumatoid Arthritis Study (ERAS) using Sequenom MassArray technology. Correlation between genetic markers and Larsen score was assessed longitudinally using zero-inflated negative binomial regression to include repeat measurements in the same individual at different timepoints. Genetic markers associated with radiological damage in ERAS were tested using the same modeling techniques on previously published data from the Norfolk Arthritis Register (NOAR).Results.The single marker associated longitudinally with Larsen score in ERAS (p = 0.02) and in NOAR (p = 0.04) was rs2900180 at the TRAF1 locus. Analysis of individual timepoints in ERAS showed that rs2900180 displays its effect primarily on the extent of Larsen score early in the disease course. Combined longitudinal analysis of the 2 cohorts suggests further association of several loci with Larsen score (KIF5A, PTPN22, AFF3, TAGAP) and therefore a significant accumulation of RA severity markers among RA susceptibility markers (p = 0.016).Conclusion.The marker rs2900180 is associated with the extent of radiological damage in the ERAS cohort. This represents the second independent study correlating rs2900180 at the TRAF1 locus with radiological severity in RA. Replication in a large dataset is required to establish the role of other RA susceptibility loci in disease severity.

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“…For detection of TRAF1 polymorphism, DNA was isolated and purified from whole blood (EDTA) using QIAamp -spin columns according to the protocol provided by the manufacturer (QIAamp DNA Blood Mini Kit). 24 Heparinized blood was used for Peripheral blood mononuclear cells isolation for IL-22 assay. In addition the separated serums were collected and stored in −80 °C until laboratory tests were done.…”

Section: Sample Collection and Analysismentioning

confidence: 99%

Interleukin-22 and Tumor Necrosis Factor Receptor Associated Factor 1 (TRAF1) in Patients with Rheumatoid Arthritis and Systemic Lupus Erythematosus: Correlation with Disease Activity

Rashwan

Moaaz

Mohannad

et al. 2015

Egypt J of Rheumatol & Clinical Immunol

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In autoimmune diseases including rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE), cytokines play a central role in initiating and maintaining diverse immune and inflammatory responses. Interleukin 22 (IL-22), a member of IL-10 cytokine family, has been believed to be an important player in regulating inflammatory responses associated with many autoimmune diseases. The aim of this study was to detect the role of IL-22 and Tumor necrosis factor receptor associated factor 1 (TRAF1) in patients with RA and SLE and their correlation with disease activity. The current study was conducted on 70 RA, 64 SLE patients and 45control subjects from Egyptian population, using ELISA to assess IL-22 in culture supernatants of cultured lymphocytes and TaqMan genotyping assay for TRAF1 (rs10818488). A significant increase in IL-22 levels in both RA and SLE patients than control group (p<0.001 for each) was detected before and after lymphocyte stimulation. Also, a significant differences in A allele frequency with RA patients was found (P=0.030) indicating that TRAF1 could be considered as a susceptibility gene to RA in the Egyptian population. The A allele of TRAF1 was significantly increased RA patients with positive rheumatoid factor (RF) (p=<0.001) and/or anti-CCP antibodies (p=0.034), this could not be demonstrated in SLE patients or controls(P=0.750). Also, IL-22 level correlated positively with disease activity in RA and SLE patients which may rise a possible role in the pathogenesis of both conditions. [Egypt J Rheumatology & Clinical Immunology, 2016; 4(1): 49-58]

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Influence of TRAF1/C5 and STAT4 genes polymorphisms on susceptibility and severity of rheumatoid arthritis in Egyptian population

Cited by 29 publications

References 35 publications

Complement Factor C5 but Not C3 Contributes Significantly to Hydrosalpinx Development in Mice Infected with Chlamydia muridarum

Complement Factor C5 but Not C3 Contributes Significantly to Hydrosalpinx Development in Mice Infected with Chlamydia muridarum

Investigation of Rheumatoid Arthritis Genetic Susceptibility Markers in the Early Rheumatoid Arthritis Study Further Replicates the TRAF1 Association with Radiological Damage

Interleukin-22 and Tumor Necrosis Factor Receptor Associated Factor 1 (TRAF1) in Patients with Rheumatoid Arthritis and Systemic Lupus Erythematosus: Correlation with Disease Activity

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