Decreased plasma IL22 levels, but not increased IL17 and IL23 levels, correlate with disease activity in patients with systemic lupus erythematosus

Cheng, F. H.; Guo, Zhiqin; Xu, Huji; Yan, Di; Li, Q

doi:10.1136/ard.2008.097089

Cited by 90 publications

(67 citation statements)

References 13 publications

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“…However, one of the seminal studies has since been retracted (30). Our results, which include a PCA, indicate that IL-17A does not exhibit discernibly different characteristics across disease activity and organ damage states, which was a similar finding to that of Zhao et al (31), Cheng et al (32), and more recently, Vincent et al (33). Furthermore, genetic studies have also been unable to establish a direct link between the IL-23/IL-17 axes and SLE (34).…”

Section: Discussionsupporting

confidence: 79%

IL-17A levels in systemic lupus erythematosus associated with inflammatory markers and lower rates of malignancy and heart damage: Evidence for a dual role

Raymond¹,

Ostli-Eilertsen²,

Griffiths³

et al. 2017

Eur J Rheumatol

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Objective: The interleukin 17 (IL-17) cytokine family is involved in a number of chronic inflammatory diseases. In spite of contradictory findings and a lack of causality in clinical studies, IL-17 inhibition for systemic lupus erythematosus (SLE) has regained attention as a potential therapeutic pathway, after demonstrating disease-modifying capabilities in ankylosing spondylitis. We investigated the clinical associations of interleukin 17 A (IL-17A) in patients with SLE.Material and Methods: A cross-sectional study was performed involving SLE patients (n=102; age: 49 years; 86% female) recruited from a regional registry. IL-17A levels were determined by immunoassay, disease activity by Systemic Lupus Erythematosus Disease Activity Index-2K (SLEDAI-2K), and cumulative damage by Systemic Lupus International Collaborative Clinics Damage Index (SDI) scores. Non-parametric techniques were used to examine the association between IL-17A and disease activity and autoantibody profiles were compared with healthy controls (n=31): principal component analysis (PCA) was used to determine the interplay of immune cells across disease states and damage development in SLE patients.Results: SLE patients had higher IgG levels, lower T-cell and B-cell counts, but median IL-17A levels did not differ from the controls (28.4 vs. 28.4 pg/mL, p=0.9). In SLE patients, IL-17A did not correlate with SLEDAI-2K or SDI, but was inversely related with age (correlation coefficients, Rs.=-0.29, p<0.05), systolic blood pressure (Rs.=-0.31, p<0.05), years of smoking (Rs.=-0.43, p<0.05), cumulative heart (Rs.=-0.22, p<0.05), and malignancy damage (Rs.=-0.18, p<0.05). Serological correlations for IL-17A existed with immunoglobulin G (IgG) levels (Rs.=0.21, p<0.05), high sensitivity C-reactive protein (hs-CRP) levels (Rs.=0.28, p<0.05), proteinuria (Rs.=0.64, p<0.05), and pre-albumin (Rs.=-0.22, p<0.05). Longitudinal data showed only modest fluctuation in IL-17A levels, independent of SLEDAI-2K. Conclusion:These results suggest that IL-17A, while participating in inflammation, may also serve a protective purpose in SLE patients.

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Section: Discussionsupporting

confidence: 79%

IL-17A levels in systemic lupus erythematosus associated with inflammatory markers and lower rates of malignancy and heart damage: Evidence for a dual role

Raymond¹,

Ostli-Eilertsen²,

Griffiths³

et al. 2017

Eur J Rheumatol

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“…In patients with active SLE, both the increase in percentage of circulating Th17 cells, [12,18,19] and elevated serum concentration of IL-17A have been described [20][21][22][23][24]. However, in some reports, no association of IL-17 with clinical markers of disease activity was found [22,23].…”

Section: Discussionmentioning

confidence: 83%

“…However, in some reports, no association of IL-17 with clinical markers of disease activity was found [22,23]. These inconsistencies are partly due to enrolment of patients regardless of the immunosuppressive therapy or at a different phase of their disease.…”

Section: Discussionmentioning

confidence: 85%

Imbalance between Th17 and regulatory T-cells in systemic lupus erythematosus

Kleczynska¹,

Jakieła²,

Plutecka³

et al. 2012

Folia Histochem Cytobiol.

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Impaired function of regulatory T-cells (Treg) leads to a failure in immune tolerance and triggers autoimmunity. We analyzed whether the deficiency in Treg in systemic lupus erythematosus (SLE) is accompanied by an increase in effector T-cell responses. We studied the frequencies of IL-17A (Th17) and IFNg (Th1) producing CD4 + T-cells by flow cytometric detection of intracellular cytokines in PMA/ionomycin stimulated blood lymphocytes from seven patients with active SLE, eight with SLE in remission, and 11 healthy controls. Circulating Treg were evaluated as CD4 + CD25 + lymphocytes expressing FoxP3. There was no difference in the percentage of Treg cells between the groups, but their absolute counts were decreased in active SLE (5 [1-7] cells/μL) compared to inactive SLE (11 [6][7][8][9][10][11][12][13][14][15]; p = 0.05) and healthy controls (16 [10-20]; p < 0.01). Both the frequency and numbers of Th1 cells were decreased in SLE compared to controls. No difference was observed in the number of Th17 cells, which resulted in a decreased Th1/Th17 ratio. In parallel, a higher Treg/Th17 ratio in healthy controls (2.2 [1.8-3.6]) compared to active SLE (1.1 [1.0-2.1]; p < 0.05) was observed. There was a correlation between the number of Treg cells and disease activity status (SLEDAI, r = -0.59). SLE patients in the active phase of the disease are characterized by a deficiency in Treg cells and decreased Treg/Th17 ratio. This suggests that the imbalance between major T-cells subsets might be responsible for an increased proinflammatory response in the exacerbation

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“…28 On the other hand, decreased serum and plasma levels of IL-22 were observed in SLE patients in a previous study. 29 There are possible reasons for this discrepancy: different cell purification techniques and possibly as suggested by Ziesche et al 30 , glucocorticoid (dexamethasone) which is the treatment given to SLE patients in the previous study can suppress IL-22 production of plasma and PBMCs. Another study carried out by Qin et al 31 showed that the percentages of IL-22 positive CD4+ T cells were increased in the PBMCs of patients with SLE compared with healthy control subjects and with a strong positive correlation to disease activity index (SLEDAI).…”

Section: Discussionmentioning

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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Decreased plasma IL22 levels, but not increased IL17 and IL23 levels, correlate with disease activity in patients with systemic lupus erythematosus

Cited by 90 publications

References 13 publications

IL-17A levels in systemic lupus erythematosus associated with inflammatory markers and lower rates of malignancy and heart damage: Evidence for a dual role

IL-17A levels in systemic lupus erythematosus associated with inflammatory markers and lower rates of malignancy and heart damage: Evidence for a dual role

Imbalance between Th17 and regulatory T-cells in systemic lupus erythematosus

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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