Increased interleukin-17 production in patients with systemic sclerosis

Kurasawa, Kazuhiro; Hirose, Koichi; Sano, Hideki; Endo, Hisayoshi; Shinkai, Hiroshi; Nawata, Yasushi; Takabayashi, Katsuhiko; Iwamoto, Itsuo

doi:10.1002/1529-0131(200011)43:11<2455::aid-anr12>3.0.co;2-k

Cited by 372 publications

(249 citation statements)

References 34 publications

Supporting

Mentioning

221

Contrasting

Unclassified

Order By: Relevance

“…There is increasing evidence that fibroblasts derived from SSc patients exhibit a fibrogenic phenotype that is capable of producing larger amounts of collagen than normal fibroblasts [2][3][4]. Recent reports on SSc emphasize the importance of cytokine and growth factor dysregulation in the overproduction of extracellular matrix of this disease [5][6][7][8][9]. The concept that T cells might play a central role in the development of tissue damage in SSc patients is also supported [10][11][12][13].…”

Section: Introductionmentioning

confidence: 99%

Increased CD40 expression in skin fibroblasts from patients with systemic sclerosis (SSc): role of CD40‐CD154 in the phenotype of SSc fibroblasts

et al. 2003

View full text Add to dashboard Cite

Systemic sclerosis (SSc) is a connective tissue disease of unknown etiology that is characterized by tissue fibrosis, which may result from the activation of lesional fibroblasts exhibiting excessive production of extracellular matrix components. However, it has yet to be determined how SSc fibroblasts are activated. CD40 is a cell surface molecule expressed on various cells that is important for the response to activated T cells through CD154. CD40 mRNA was found to be constitutively expressed in both SSc and normal fibroblasts by reverse transcription PCR. Expression of CD40 protein was increased on SSc fibroblasts compared to normal fibroblasts as measured by flow cytometry. Ligation of CD40 by recombinant human CD154 (0.5–2 μg/ml) resulted in increased production of IL‐6, IL‐8, and monocyte chemoattractant protein‐1 in SSc fibroblasts in a dose‐dependent manner, whereas these phenomena were not shown in normal fibroblasts even with the addition of CD154. CD80, a costimulatory molecule, was also induced on SSc fibroblasts by CD40 ligation. In the present study, our findings suggest the possibility of a cell‐mediated response between fibroblasts and T cells in the lesional skin of SSc patients. Since it is suggested that the CD40‐CD154 system may play a crucial role in the aberrant production of immune mediators by SSc fibroblasts, blockage of CD40‐CD154 may be a novel therapeutic strategy for SSc.

show abstract

Section: Introductionmentioning

confidence: 99%

Increased CD40 expression in skin fibroblasts from patients with systemic sclerosis (SSc): role of CD40‐CD154 in the phenotype of SSc fibroblasts

et al. 2003

View full text Add to dashboard Cite

show abstract

“…This cytokine may play a role in T cell-triggered inflammation by stimulating stromal cells to secrete various cytokines and growth factors associated with inflammation (1)(2)(3)(4). A pathogenic role for IL-17 was found in organ allograft rejection (5), and increased IL-17 expression was detected in several diseases, such as systemic sclerosis (6), nephrotic syndrome (7), systemic lupus erythematosus (8), and rheumatoid arthritis (RA) (9,10). In contrast with the restricted expression of IL-17, the IL-17 receptor is ubiquitously expressed in virtually all cells and tissues.…”

mentioning

confidence: 99%

Treatment with a neutralizing anti‐murine interleukin‐17 antibody after the onset of collagen‐induced arthritis reduces joint inflammation, cartilage destruction, and bone erosion

Lubberts¹,

Koenders²,

Oppers‐Walgreen³

et al. 2004

Arthritis & Rheumatism

653

456

View full text Add to dashboard Cite

Objective. Interleukin-17 (IL-17) is a proinflammatory cytokine that is expressed in the synovium of rheumatoid arthritis (RA) patients. This T cell cytokine is implicated in the initiation phase of arthritis. However, the role of IL-17 during the effector phase of arthritis has still not been identified; this was the objective of the present study.Methods. Mice with collagen-induced arthritis (CIA) were treated with polyclonal rabbit anti-murine IL-17 (anti-IL-17) antibody-positive serum or normal rabbit serum after the first signs of arthritis. In addition, during a later stage of CIA mice were selected and treated with anti-IL-17 antibody or control serum. Arthritis was monitored visually, and joint pathology was examined radiologically and histologically. Systemic IL-6 levels were measured by enzyme-linked immunosorbent assay, and local synovial IL-1 and receptor activator of NF-B ligand (RANKL) expression was analyzed using specific immunohistochemistry.Results

show abstract

“…For example, serum IL-17 levels are abnormally elevated in patients with lupus (14,15); IL-17 could act in synergy with B cellactivating factor to affect B cell biology and the pathophysiology of SLE (16). However, the most direct evidence came from a study by Kyttaris et al, who reported that IL-23 receptor-deficient B6/lpr mice display decreased numbers of double-negative T cells and IL-17-producing cells and fewer anti-DNA antibodies (17).…”

mentioning

confidence: 99%

Oral administration of artemisinin analog SM934 ameliorates lupus syndromes in MRL/lpr mice by inhibiting Th1 and Th17 cell responses

Hou¹,

He²,

Li³

et al. 2011

Arthritis & Rheumatism

106

View full text Add to dashboard Cite

Objective. SM934, an artemisinin derivative, possesses potent antiproliferative and antiinflammatory properties. The aim of this study was to examine the effects and explore the mechanisms of SM934 to treat autoimmune disease in lupus-prone female MRL/lpr mice.Methods. In vitro, the effects of SM934 on the activation of polyclonal CD4؉ T cells and the differentiation of naive CD4؉ T cells were examined. In vivo, the preventative or therapeutic effects of SM934 in MRL/lpr mice were investigated. Ex vivo, the mechanisms of treatment were explored according to the immunologic correlates of disease.Results In female MRL/lpr mice, an autoimmune syndrome develops spontaneously that closely resembles human systemic lupus erythematosus (SLE) and is characterized by the production of various autoantibodies and the development of fatal glomerulonephritis (1,2).Disease begins as early as 8 weeks of age in these mice, with the presence of detectable serum autoantibodies. Pronounced lymphadenopathy is observed at 12 weeks of age, which is largely attributable to the accumulation of a population of B220ϩ and CD3ϩ cells that are mostly CD4Ϫ and CD8Ϫ (double-negative T cells). By 12-16 weeks of age, MRL/lpr mice begin to produce a variety of autoantibodies, including antidouble-stranded DNA (anti-dsDNA) antibodies. Multiple organs are affected, and a steady deterioration of renal function manifesting as severe proteinuria begins at approximately 16 weeks of age. From 16 weeks of age to 24 weeks of age, proliferative immune complex-

show abstract

Increased interleukin-17 production in patients with systemic sclerosis

Cited by 372 publications

References 34 publications

Increased CD40 expression in skin fibroblasts from patients with systemic sclerosis (SSc): role of CD40‐CD154 in the phenotype of SSc fibroblasts

Increased CD40 expression in skin fibroblasts from patients with systemic sclerosis (SSc): role of CD40‐CD154 in the phenotype of SSc fibroblasts

Treatment with a neutralizing anti‐murine interleukin‐17 antibody after the onset of collagen‐induced arthritis reduces joint inflammation, cartilage destruction, and bone erosion

Oral administration of artemisinin analog SM934 ameliorates lupus syndromes in MRL/lpr mice by inhibiting Th1 and Th17 cell responses

Contact Info

Product

Resources

About