IL-20-Receptor Signaling Delimits IL-17 Production in Psoriatic Inflammation

Ha, Hojin; Wang, Hongshan; Claudio, Estefanı́a; Tang, Wanhu; Siebenlist, Ulrich

doi:10.1016/j.jid.2019.06.127

Cited by 15 publications

(8 citation statements)

References 37 publications

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“…Monocyte chemoattractant protein-1 (MCP-1) is one of the key chemokines that regulates infiltration of monocytes/macrophages [ 36 ]. A previous study showed that IL-20 controlled T cell infiltration by regulating the expression of MCP-1 in mouse psoriasis models [ 19 ]. Thus, we investigated whether IL-20 affects MCP-1 expression and CD11b-positive macrophage infiltration in mice alveolar bone during OTM.…”

Section: Resultsmentioning

confidence: 99%

“…Several bone-affecting inflammatory cytokines such as TNF, IL-1, IL-6, IL-17, IL-22, IL-23 and IL-33, secreted by immune cells, synergistically act with RANKL and disrupt the balance of bone resorption and bone formation, leading to bone homeostasis disorders in bone loss diseases [ 7 , 8 , 9 , 10 ]. Interestingly, most of the above-mentioned cytokines are regulated by IL-20, one of the IL-20 subfamily cytokines that belongs to the IL-10 large family [ 11 , 12 , 13 , 14 , 15 , 16 , 17 , 18 , 19 , 20 , 21 ]. IL-20 is mainly produced by activated macrophages and skin cells [ 22 , 23 ].…”

Section: Introductionmentioning

confidence: 99%

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Dual Role of Interleukin-20 in Different Stages of Osteoclast Differentiation and Its Osteoimmune Regulation during Alveolar Bone Remodeling

Meng

Yang

et al. 2023

IJMS

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Osteoimmunology mediators are critical to balance osteoblastogenesis and osteoclastogenesis to maintain bone homeostasis. A lot of the osteoimmunology mediators are regulated by interleukin-20 (IL-20). However, little is known about the role of IL-20 in bone remodeling. Here, we showed that IL-20 expression was correlated with osteoclast (OC) activity in remodeled alveolar bone during orthodontic tooth movement (OTM). Ovariectomize (OVX) in rats promoted OC activity and enhanced IL-20 expression, while blocking OC inhibited IL-20 expression in osteoclasts. In vitro, IL-20 treatment promoted survival, inhibited apoptosis of the preosteoclast at the early stages of osteoclast differentiation, and boosted the formation of osteoclasts and their bone resorption function at the late stages. More importantly, anti-IL-20 antibody treatment blocked IL-20-induced osteoclastogenesis and the subsequent bone resorption function. Mechanistically, we showed that IL-20 synergistically acts with RANKL to activate the NF-κB signaling pathway to promote the expression of c-Fos and NFATc1 to promote osteoclastogenesis. Moreover, we found that local injection of IL-20 or anti-IL-20 antibody enhanced osteoclast activity and accelerated OTM in rats, while blocking IL-20 reversed this phenomenon. This study revealed a previously unknown role of IL-20 in regulating alveolar bone remodeling and implies the application of IL-20 to accelerated OTM.

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Section: Resultsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Dual Role of Interleukin-20 in Different Stages of Osteoclast Differentiation and Its Osteoimmune Regulation during Alveolar Bone Remodeling

Meng

Yang

et al. 2023

IJMS

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“…For instance, knockdown of mouse IL-20R (an IL-24 receptor subunit) has been shown to limit IL-17A-producing dermal γδ T-cell accumulation and Th17 responses in psoriatic inflammation. 27 Higher rather than lower concentrations of IL-24 were found to increase the Th1 frequency and T-bet mRNA levels, but not the Th17 or RORγt mRNA levels, in colorectal adenocarcinoma. 28 In fact, T cells and other immune cells do not express IL-24-related receptors, indicating that immune cells are unlikely to the target cells of IL-24.…”

Section: Discussionmentioning

confidence: 88%

IL-24 Contributes to Neutrophilic Asthma in an IL-17A-Dependent Manner and Is Suppressed by IL-37

Feng

Meng

Zhang

et al. 2022

Allergy Asthma Immunol Res

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Purpose Neutrophilic asthma is associated with asthma exacerbation, steroid insensitivity, and severe asthma. Interleukin (IL)-24 is overexpressed in asthma and is involved in the pathogenesis of several allergic inflammatory diseases. However, the role and specific mechanism of IL-24 in neutrophilic asthma are unclear. We aimed to elucidate the roles of IL-24 and IL-37 in neutrophilic asthma, the relationships with IL-17A and the mechanisms regulating neutrophilic asthma progression. Methods Purified human neutrophils were isolated from healthy volunteers, and a cell coculture system was used to evaluate the function of IL-24 in epithelium-derived IL-17A-dependent neutrophil migration. IL-37 or a small interfering RNA (siRNA) targeting IL-24 was delivered intranasally to verify the effect in a murine model of house dust mite (HDM)/lipopolysaccharide (LPS)-induced neutrophilic asthma. Results IL-24 enhanced IL-17A production in bronchial epithelial cells via the STAT3 and ERK1/2 signaling pathways; this effect was reversed by exogenous IL-37. Anti-IL-17A monoclonal antibodies reduced neutrophil chemotaxis induced by IL-24-treated epithelial cells in vitro . Increased IL-24 and IL-17A expression in the airway epithelium was observed in HDM/LPS-induced neutrophilic asthma. IL-37 administration or IL-24 silencing attenuated neutrophilic asthma, reducing IL-17A levels and decreasing neutrophil airway infiltration, airway hyperresponsiveness, and goblet cell metaplasia. Silencing IL-24 inhibited T-helper 17 (Th17) immune responses, but not Th1 or Th2 immune responses, in the lungs of a neutrophilic asthma model. Conclusions IL-24 aggravated neutrophilic airway inflammation by increasing epithelium-derived IL-17A production, which could be suppressed by IL-37. Targeting the IL-24/IL-17A signaling axis is a potential strategy, and IL-37 is a potential candidate agent for alleviating neutrophilic airway inflammation in asthma.

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“…With the initial description of the imiquimod (IMQ) inducible model of psoriasis (van der Fits et al, 2009) and cytokine injection models (Zheng et al, 2007), acute or inducible models have rapidly become one of the most widely used systems for studying human psoriasis (Hawkes et al, 2018). Recent examples of the utilization of this model include the demonstration of IL-1b/IL-1R signaling pathway in skin inflammation (Cai et al, 2019); therapeutic intervention to determine the response to topical tacrolimus (Pischon et al, 2018); link between skin inflammation and hyperglycemia (Ikumi et al, 2019); role of IL-20 receptor signaling (Ha et al, 2019) and IL-17E (Senra et al, 2019) in psoriasis pathogenesis; and to elucidate the function of Trim32 in psoriasis and atopic dermatitis (Liu et al, 2017). However, some concerns have been raised about the overutilization of this model and its variability depending on the mouse strain used (Swindell et al, 2017).…”

Section: Modeling Of Psoriasis E Mouse Models and Beyondmentioning

confidence: 99%