Behcet's disease is a chronic multisystemic disease with remissions and relapses. Several studies have shown that immune mechanisms play an important role in the development of the disease. In order to assess the association of disease activity with IL-17A/F, IL-23, IL-12/23 (p40) and IL-35 expression, we aimed to investigate production of these cytokines in peripheral blood mononuclear cells (PBMCs) from Behcet's patients and normal controls. Furthermore, we included Systemic Lupus Erythematosus (SLE) as disease control to evaluate the specificity of our data for immunopathogenesis of BD. Totally 15 active, 15 inactive Behcet's patients, 12 active and 12 inactive SLE patients and 12 healthy volunteers were enrolled in the study. Peripheral blood mononuclear cells were separated, lymphocyte cultures were performed and IL-17A/F, IL-12/23 p(40), IL-23, IL-35 cytokine levels were measured by ELISA in culture supernatants in the presence or absence of phytohemagglutinin (PHA) on time-dependent manner. IL-17 A/F levels increased parallel to IL-23 levels in Behcet's and SLE patients. Compared to healthy controls, IL-17 A/F levels were higher in active Behcet's and SLE patients; on the contrary, levels of IL-35 were lower. IL-17A/F, IL-12/23 (p40) and IL-23 levels were detectable most frequently in active Behcet's patients followed by active SLE patients. Our results indicate that IL-17 A/F, IL-23 and IL-12/23 (p40) may play role in the immunopathogenesis of BD so as Th17 and Th1 cell responses. Since IL-35 levels were lower in active Behcet's patients compared to inactive patients and healthy controls, there may be a plasticity between Th17 and Treg cells according to the state of disease activity.
Aim: Autoantibody development plays an important role in the pathogenesis of systemic lupus erythematosus (SLE) and rheumatoid arthritis (RA). In this study, we aimed to determine the diagnostic value of anticarbamylated protein antibody (anti-CarP) antibody in SLE and RA patients and its relationship with disease prognosis. Material & method: Fifty-seven SLE patients (F/M 50/7; median age 40.9 ± 13.7; median disease duration 2 years) who met the 2012 SLICC SLE diagnostic criteria were included in the study. A total of 46 RA patients selected according to the 2010 ACR/EULAR diagnostic criteria (F/M 38/8; median age 54.2 ± 12.4; median disease duration 2 years) were included. A total of 30 healthy individuals were selected as the control group. The anti-CarP antibody was studied by using human anticarbamylated protein antibody ELISA Kit (SunRedBio, Shanghai, China). Results: Anti-CarP antibody positivity was found to be 17.4% in RA patients (p < 0.001), 54.4% in SLE patients (p < 0.001) and 3.3% in the healthy control group. The anti-CarP antibody was determined to predict SLE patients with 54.4% sensitivity and 96.7% specificity compared with the healthy control group (area under the curve: 0.755; p < 0.001). Conclusion: Anti-CarP antibody positivity was significantly higher in the SLE patients compared with the healthy control and RA group. It has significant sensitivity and specificity in both SLE and RA patients compared with the healthy controls.
BackgroundSystemic lupus erythematosus (SLE) is a chronic systemic autoimmune disease characterised by numerous organ involvement. In SLE, autoantibody development against nucleic acids and their binding proteins plays an important role in disease pathogenesis.ObjectivesPurpose of this study is the determination of the diagnostic value of anti-carbamyl antibody in patients with Systemic Lupus Erythematosus and rheumatoid arthritis and the relationship with disease prognosis.MethodsFifty-seven SLE patients (F/M 50/7; median age 40.9±13.7; median disease duration 2 years) were included in the study according to the 2012 SLICC SLE diagnostic criteria. 46 RA patients (F/M 38/8, median age 54.2±12.4 years, the median duration of disease 2 years) selected according to 2010 ACR/EULAR diagnostic criteria were included. 30 healthy control groups were selected. Anti carP antibody Anti-carbamylated Protein Human anti-carbamylated Protein Antibody (ACP-Ab) ELISA Kit (SunRedBio, China) was used for measurement of antibodies against carbamylated proteins.ResultsThe study population consisted of 133 subjects, 30 controls, 57 SLEs and 46 RAs. The mean age of SLE patients was lower than that of RA patients. (40,9±13,7 versus 54,2±12,4; p<0,001). The proportion of active smokers was found to be higher in RA patients compared to SLE patients (19.6% versus 5.3%, p=0.005). The frequency of anti carP antibody positivity was 3.3% in the healthy control group. In contrast, the frequency of anti carP antibody positivity was found as high as 17.4% in patients with RA. (p=<0.001), And this frequency was 54.4% in the SLE patient group (p=<0.001) Anti carP antibody predicted SLE patients with 54.4% sensitivity and 96.7% specificity compared to the healthy control group. (AUC: 0.755, p<0.001) Anti carP antibody predicted RA patients with 17.4% sensitivity and 96.7% specificity compared to the healthy control group (AUC: 0.570, p=0.032). Anti carP antibody predicted SLE patients with 54.5% sensitivity and 82.6% specificity compared to healthy RA group (AUC: 0.685, p<0.001). AnticarP antibodies were found to be positive in all of the SLE patient groups with anti-CCP positivity. There was no significant difference in terms of in organ involvement between anti-carp antibody positive or negative SLE patients. Anti-carP antibody positivity was assessed by ROC Curve analysis for the prediction of diagnostic performance in SLE patients compared to RA patients. Accordingly, Anti carP antibody positivity, ANA positivity, were found to have similar diagnostic performance. (AUC: 0.639)Abstract THU0345 – Table 1Anti carbamylated protein antibody positivity distribution across groupsConclusionsAntibody positivity was found to be 54.4% in SLE patient group. It is significantly higher in SLE compared to healthy control and RA patient group. In the SLE group, it is still a more significant diagnostic prognostic than the healthy control and RA group. Both SLE and RA patients have significant sensitivity and specificity compared to the healthy control group.Disc...
Exact pathogenesis of Behcet’s Disease (BD) hasn’t been known but recent studies suggest it’s a genetic-based and immune-related disease. We aimed to investigate the association between disease activity and Th1, Th17 and Treg cells in BD patients via IL-17A/F, IL-23, IL-12/23p40, IL-35 produced by these cells. We also compared our findings with those of SLE patients to investigate their specificity for immunopathogenesis of BD. 15 active and 15 inactive BD patients, 12 active and 12 inactive SLE patients and 12 sex & age-matched healthy controls were involved. Peripheral blood lymphocyte cultures were done. Supernatants from PHA-stimulated and -unstimulated cultures were measured for IL-17A/F, IL-12/23p40, IL-23 and IL-35 levels in time-dependent manner (48 and 72 hrs) by ELISA. For disease activity International Study Group Diagnostic Criteria and SLEDAI index were used for BD and SLE, respectively. IL-17 and IL-23 increased parallelly in both BD and SLE; IL-17 was higher but another Treg cytokine IL-35 was lower in active BD and active SLE compared to healthy controls. After 48 and 72 hrs of PHA stimulation the highest levels of IL-17A/F, IL-22723p40 and IL-23 were measured in active BD followed by active SLE. Our data suggest that IL-17, IL-23 and IL-12/23p40; Th17 and Th1 responses play role in pathogenesis of BD. Finding IL-35 to be lower in active BD compared to inactive BD patients and healthy controls made us think that there can be a plasticity between Th17 and Treg cells depending on disease activity. This is the first time such plasticity is suggested for BD in literature. Our findings also show that IL-17/23 axis contributes to pathogenesis of SLE (another inflammatory rheumatic disease) in addition to other mechanisms like in BD.
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