Gene expression of cytokines (TNF-α, IFN-γ), serum profiles of IL-17 and IL-23 in paediatric systemic lupus erythematosus

Rana, Anita; Minz, RW; Aggarwal, Ritu; Anand, Shashi; Pasricha, Neelam; Singh, Surjit

doi:10.1177/0961203312451200

Cited by 78 publications

(82 citation statements)

References 36 publications

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“…In the ALPS and DALD patients, the defective function of Fas may further increase this resistance to apoptosis and may favor the expansion of this T-cell subset and the increased levels of IL-17s, which may in turn favor the development of autoimmunity. This mechanism may also play a role in other autoimmune diseases because high levels of IL-17 similar to that detected in our patients have been described in SLE, 24,28 RA, 29,30 and psoriasis. [31][32][33] Moreover, decreased Fas function has been also detected in patients displaying autoimmune diseases different from ALPS and DALD.…”

Section: Discussionsupporting

confidence: 86%

IL-17 protects T cells from apoptosis and contributes to development of ALPS-like phenotypes

Boggio

Clemente

Mondino

et al. 2014

Blood

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Section: Discussionsupporting

confidence: 86%

IL-17 protects T cells from apoptosis and contributes to development of ALPS-like phenotypes

Boggio

Clemente

Mondino

et al. 2014

Blood

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“…In addition to IL-17, IL-23 was also found to be crucial for the development of various autoimmune diseases in murine models [40–42] and in humans [43] by promoting Th17 cell–mediated tissue inflammation. There is accumulating evidence indicating the importance of IL-23 in patients with SLE [44–46]. Of note, our group has shown that clinical and pathology findings of LN are mitigated in lupus prone mice with IL-23 receptor deficiency [47] or treated with an anti-IL23 antibody [48].…”

Section: Il-17 In Slementioning

confidence: 99%

T cells and IL-17 in lupus nephritis

Koga

Ichinose

Tsokos

2017

Clinical Immunology

108

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Systemic lupus erythematosus (SLE) is a complicated autoimmune disorder characterized by autoantibodies production, immune complex formation, and immune dysregulation, resulting in damage of multiple organs including the kidney. Lupus nephritis (LN) is the most common severe manifestation of SLE involving the majority of patients. Even though there are a number of reports indicating that interleukin-17 (IL-17) and Th17 cells play important roles in the pathogenesis of LN, the precise molecular mechanisms underline the development of LN have not been totally elucidated. In this review, we briefly summarize general characteristics of T and IL-17 cells in SLE. In addition, we discuss in detail T cell signaling pathways which control IL-17 production in patients with LN and in glomerulonephritis in lupus-prone mice. A better understanding of signaling and gene regulation defects in LN will lead to the identification of novel therapeutic targets and predictive biomarkers for diagnosis and prognosis of this disease.

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“…Studies have shown different cytokine profiles for Th1, Th2, Th17, and Treg cells in adult SLE patients compared to a healthy control group, as well as differences in disease phenotype and activity (7–12). However, only a few studies have investigated the cytokine profile of cSLE (13–16). Therefore, we conducted a cross-sectional and longitudinal study to determine the profiles of IL-2, IL-4, IL-6, IL-10, IL-17A, IFN-γ, and TNF cytokines in cSLE patients and a healthy control group, and evaluated the association of these cytokines with disease activity.…”

Section: Introductionmentioning

confidence: 99%

Cytokine profile in childhood-onset systemic lupus erythematosus: a cross-sectional and longitudinal study

Cavalcanti

Santos

Mesquita

et al. 2017

Braz J Med Biol Res

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Childhood-onset systemic lupus erythematosus (cSLE) exhibits an aggressive clinical phenotype and severe complications. This could be due to a pro-inflammatory cytokine milieu. Therefore, we determined plasma levels of Th1 (IL-2, IFN-γ, TNF), Th2 (IL-4), Th17 (IL-17A, IL-6), and Treg (IL-10) cytokines in a cohort of cSLE patients and healthy controls, and we evaluated the association between these cytokines and disease activity. We conducted a cross-sectional study with 51 cSLE patients from two pediatric rheumatology services. Ten cSLE patients participated in a longitudinal follow-up study. Blood samples were collected from the same patient during active and inactive disease. Disease activity was evaluated according to SLE Disease Activity Index 2000 (SLEDAI-2K). Cytokines levels were measured by cytometric bead array technique. cSLE patients had higher IL-6 (P<0.001) and IL-10 (P<0.001) levels than healthy controls. Patients with active disease had higher IL-6 and IL-10 levels than patients with inactive disease (P=0.001 and P=0.014, respectively) and the control group (both P<0.001). IL-6 (P=0.022), IL-10 (P=0.013), and IL-17A (P=0.041) levels were significantly higher during active than inactive disease. Linear regression analysis revealed IL-6 (P=0.002, 95%CI=0.006-0.025) and IL-10 (P=0.01 95%CI=0.021-0.150) as independent factors for increased SLEDAI-2K. IL-6, IL-10, and IL-17A are candidate biomarkers for disease activity in cSLE patients. This is the first longitudinal study to support their pivotal role in the pathogenesis of the disease.

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Gene expression of cytokines (TNF-α, IFN-γ), serum profiles of IL-17 and IL-23 in paediatric systemic lupus erythematosus

Cited by 78 publications

References 36 publications

IL-17 protects T cells from apoptosis and contributes to development of ALPS-like phenotypes

IL-17 protects T cells from apoptosis and contributes to development of ALPS-like phenotypes

T cells and IL-17 in lupus nephritis

Cytokine profile in childhood-onset systemic lupus erythematosus: a cross-sectional and longitudinal study

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