IL-17A- versus IL-17F-induced intracellular signal transduction pathways and modulation by IL-17RA and IL-17RC RNA interference in rheumatoid synoviocytes

Hot, A.; Zrioual, Saloua; Toh, Myew–Ling; Lenief, Vanina; Miossec, Pierre

doi:10.1136/ard.2010.132233

Cited by 66 publications

(63 citation statements)

References 29 publications

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“…Microarray analysis of IL-17A-induced mRNA expression in RA synoviocytes showed the activation of several pathways as previously reported elsewhere 14 15. Using database, literature knowledge and IPA analysis, genes were identified as involved in the response to hypoxia.…”

Section: Resultssupporting

confidence: 58%

IL-17 and tumour necrosis factor α combination induces a HIF-1α-dependent invasive phenotype in synoviocytes

Hot

Zrioual²,

Lenief³

et al. 2012

Ann Rheum Dis

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Section: Resultssupporting

confidence: 58%

IL-17 and tumour necrosis factor α combination induces a HIF-1α-dependent invasive phenotype in synoviocytes

Hot

Zrioual²,

Lenief³

et al. 2012

Ann Rheum Dis

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“…IL-17 enhances production of inflammatory cytokines and chemokines from RA synoviocytes (38). Furthermore, deficiency of IL-17 is reported to inhibit murine CIA (33).…”

Section: Discussionmentioning

confidence: 99%

Necessity of Lysophosphatidic Acid Receptor 1 for Development of Arthritis

Miyabe

Iwai

et al. 2013

Arthritis & Rheumatism

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Objective. Lysophosphatidic acid (LPA) is a bioactive lipid that binds to a group of cell surface G protein-coupled receptors (LPA receptors 1-6 [LPA 1-6 ]) and has been implicated as an important mediator of angiogenesis, inflammation, and cancer growth. This study was undertaken to analyze the effects of LPA 1 on the development of arthritis.Methods. Expression of LPA receptors on synovial tissue was analyzed by immunohistochemistry and quantitative reverse transcription-polymerase chain reaction. The effects of abrogation of LPA 1 on collageninduced arthritis (CIA) were evaluated using LPA 1 -deficient mice or LPA 1 antagonist. Migrating fluorescence-labeled CD11b؉ splenocytes, which were transferred into the synovium of mice with CIA, were counted. CD4؉ naive T cells were incubated under Th1-, Th2-, or Th17-polarizing conditions, and T helper cell differentiation was assessed. Osteoclast formation from bone marrow cells was examined.Results. LPA 1 was highly expressed in the synovium of patients with rheumatoid arthritis (RA) compared with that of patients with osteoarthritis. LPA 1 -deficient mice did not develop arthritis following immunization with type II collagen (CII). LPA 1 antagonist also ameliorated murine CIA. Abrogation of LPA 1 was associated with reductions in cell infiltration, bone destruction in the joints, and interleukin-17 production from CII-stimulated splenocytes. Infiltration of transferred CD11b؉ macrophages from LPA 1 -deficient mice into the synovium was suppressed compared with infiltration of macrophages from wild-type mice. LPA 1 antagonist inhibited the infiltration of macrophages from wild-type mice. Differentiation into Th17, but not Th1 or Th2, and osteoclast formation were also suppressed under conditions of LPA 1 deficiency or LPA 1 inhibition in vitro.Conclusion. Collectively, these results indicate that LPA/LPA 1 signaling contributes to the development of arthritis via cellular infiltration, Th17 differentiation, and osteoclastogenesis. Thus, LPA 1 may be a promising target molecule for RA therapy.Rheumatoid arthritis (RA) is a chronic inflammatory disease characterized by inflammatory cell infiltration and bone destruction at multiple joints. The inflammation process in RA leads to synovial hyperplasia with proliferation of fibroblast-like synoviocytes (FLS), angiogenesis, and infiltration of inflammatory cells, including lymphocytes and macrophages (1,2).

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“…This pro-inflammatory cytokine produced by the Th17 T cell subset has pleiotropic activities, including the induction of other inflammatory cytokines (eg, IL-6, TNFα, IL-1β), chemokines (CCL20 and IL-8), adhesion molecules (eg, ICAM-1) and pro-inflammatory mediators (prostaglandin E 2 , nitric oxide and cyclooxygenase-2) in synoviocytes, a cell critical for the local pathogenesis of RA 6–8…”

mentioning

confidence: 99%

Combination of IL-17 and TNFα induces a pro-inflammatory, pro-coagulant and pro-thrombotic phenotype in human endothelial cells

2012

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IL-17A- versus IL-17F-induced intracellular signal transduction pathways and modulation by IL-17RA and IL-17RC RNA interference in rheumatoid synoviocytes

Abstract: Like IL-17A, IL-17F regulates proinflammatory gene expression by a very similar but not identical signalling pathway involving IL-17RA and IL-17RC.

Cited by 66 publications

References 29 publications

IL-17 and tumour necrosis factor α combination induces a HIF-1α-dependent invasive phenotype in synoviocytes

IL-17 and tumour necrosis factor α combination induces a HIF-1α-dependent invasive phenotype in synoviocytes

Necessity of Lysophosphatidic Acid Receptor 1 for Development of Arthritis

Combination of IL-17 and TNFα induces a pro-inflammatory, pro-coagulant and pro-thrombotic phenotype in human endothelial cells

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