Tumor Necrosis Factor α-Mediated Induction of Interleukin 17C in Human Keratinocytes Is Controlled by Nuclear Factor κB

Johansen, Claus; Riis, Jette Lindorff; Gedebjerg, Anne; Kragballe, Knud; Iversen, Lars

doi:10.1074/jbc.m111.240671

Cited by 53 publications

(49 citation statements)

References 43 publications

(39 reference statements)

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“…6 A hypothesis of a positive feedback loop between the expression of IL-17C and the activation of macrophages. The expression of IL-17C in macrophages was identified [23,26] and further supported in this study. And the direct proinflammatory effect of IL-17C on macrophages was also identified [22,26,34].…”

Section: Il-17c Immunofluorescencesupporting

confidence: 59%

“…Discussion IL-17C is a novel proinflammatory cytokine that is involved in many inflammatory diseases, including rheumatoid [28] and psoriatic conditions [24,29] and conditions under the compressive force [25]. Interleukin-17C has also been proven to originate from several sources, including human keratinocytes [23], MC3T3-E1 cells [25] [26], synovial fluid mononuclear cells of rheumatoid arthritis patients [28] and Fig. 5 The semiquantitative analysis for the aseptic loosening, rheumatoid arthritis and the negative control groups.…”

Section: Il-17c Immunofluorescencementioning

confidence: 99%

“…including macrophages, rather than T cells [23][24][25][26][27]. IL-17C was demonstrated to have strong proinflammatory effects [26].…”

Section: Introductionmentioning

confidence: 99%

“…And IL-17C was found to contribute to the exacerbation of the inflammation by increasing TNF-alpha and IL-1beta expression [22,26]. In humans, IL-17C has been identified to be expressed in the synovial cells of rheumatoid arthritis patients [28], in psoriatic skin [24,29], and in cultured human keratinocytes stimulated with TNF-alpha [23]. However, little is known about the expression of IL-17C in other diseases characterised by macrophage infiltration, such as the aseptic loosening after joint arthroplasty.…”

Section: Introductionmentioning

confidence: 99%

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Presence of interleukin-17C in the tissue around aseptic loosened implants

Hou

Zhang

et al. 2013

International Orthopaedics (SICOT)

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Purpose The most common long-term complication of joint arthroplasty is aseptic loosening. The proinflammatory cytokines secreted by macrophages are involved in aseptic loosening. Recently, a novel proinflammatory cytokine IL-17C was reported to participate in inflammatory diseases by synergising with proinflammatory cytokines. However, the relationship between IL-17C and the aseptic loosening is unclear. Methods The tissues around aseptic loosened implants were collected during revision surgery and handled by formalin fixation and embedded in paraffin. The presence of IL-17C in the tissues around the aseptic loosened implants was investigated in 12 aseptic loosening patients using immunofluorescence. Results The presence of IL-17C protein in the tissues around aseptic loosened implants was detected by immunofluorescence. There are no statistical differences between optical density of IL-17C in aseptic loosening samples and in rheumatoid arthritis samples (positive control). Conclusions These results suggest the presence of IL-17C in aseptic loosening. Interleukin-17C was related to the inflammation of aseptic loosening, possibly by contributing to the inflammation and osteolysis in the tissues surrounding aseptic loosened implants.

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Section: Il-17c Immunofluorescencesupporting

confidence: 59%

Section: Il-17c Immunofluorescencementioning

confidence: 99%

“…including macrophages, rather than T cells [23][24][25][26][27]. IL-17C was demonstrated to have strong proinflammatory effects [26].…”

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Presence of interleukin-17C in the tissue around aseptic loosened implants

Hou

Zhang

et al. 2013

International Orthopaedics (SICOT)

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“…In addition to TLRs and inflammatory cytokine signaling, the transcription factor NF-κB is likely to control the transcriptional activation of the Il17c gene. 169 TNFα also cooperates with IL-17 to amplify IL-17C expression in intestinal epithelial cells; this synergistic effect requires TNFα-induced NF-κB, ERK and P38 expression and IL-17-induced AKT and C/EBPδ activation. 170 Similar to IL-17, IL-17C induces inflammatory gene and antimicrobial peptide expression either alone or in synergy with IL-22, indicating that IL-17C signaling maybe critical for the host defense response.…”

Section: Il-17cmentioning

confidence: 99%

The roles and functional mechanisms of interleukin-17 family cytokines in mucosal immunity

et al. 2016

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The mucosal immune system serves as our front-line defense against pathogens. It also tightly maintains immune tolerance to self-symbiotic bacteria, which are usually called commensals. Sensing both types of microorganisms is modulated by signalling primarily through various pattern-recognition receptors (PRRs) on barrier epithelial cells or immune cells. After sensing, proinflammatory molecules such as cytokines are released by these cells to mediate either defensive or tolerant responses. The interleukin-17 (IL-17) family members belong to a newly characterized cytokine subset that is critical for the maintenance of mucosal homeostasis. In this review, we will summarize recent progress on the diverse functions and signals of this family of cytokines at different mucosal edges.

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LncRNA UCA1 negatively regulates NF‐kB activity in psoriatic keratinocytes through the miR125a‐A20 axis

Wen

Cong

et al. 2021

The Kaohsiung J of Med Scie

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Psoriasis is one of the most common chronic inflammatory skin diseases that affects approximately 3% of the world's population. Hyper proliferation, infiltration of inflammatory cells and aberrant differentiation of keratinocytes are the three most important characteristics of psoriasis. Previous reports showed that NF‐κBis the crucial mediator linking psoriatic keratinocytes and immune cell states through its effects on chemokine and cytokine production. To identify the role of NF‐κB in psoriasis, we conducted ELISA assay to detect the activity of NF‐κB in lesional skin and nonlesional skin of patients with psoriasis. Mounting evidence suggests that the interaction between long noncoding RNAs (lncRNAs) and microRNAs plays important role in the regulation of the initiation and development of various diseases. In this article, we identified that lncRNA UCA1 was down‐regulated in lesional skin of patients with psoriasis. Further studies showed that lncRNA UCA1 could promote the expression of A20 by inhibitingmiR125a, and up‐regulated A20 decreased the activity of NF‐κB through its ubiquitin editing function. Taken together, we identified and demonstrated that lncRNA UCA1 negatively regulated NF‐κB activity in psoriasis through the miR125a‐A20 axis.

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Tumor Necrosis Factor α-Mediated Induction of Interleukin 17C in Human Keratinocytes Is Controlled by Nuclear Factor κB

Cited by 53 publications

References 43 publications

Presence of interleukin-17C in the tissue around aseptic loosened implants

Presence of interleukin-17C in the tissue around aseptic loosened implants

The roles and functional mechanisms of interleukin-17 family cytokines in mucosal immunity

LncRNA UCA1 negatively regulates NF‐kB activity in psoriatic keratinocytes through the miR125a‐A20 axis

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