Differential regulation of IL-23 production in M1 macrophages by TIR8/SIGIRR through TLR4- or TLR7/8-mediated signaling

Yamaguchi, Rui; Sakamoto, Arisa; Yamamoto, Tomohisa; Narahara, Sayoko; Sugiuchi, Hiroyuki; Yamaguchi, Yasuo

doi:10.1016/j.cyto.2017.08.014

Cited by 18 publications

(12 citation statements)

References 28 publications

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“…IL-6 has been shown to promote Th17 and γδT-cell differentiation in combination with TGF-β [22,137]. These two cell populations produce IL-17 upon stimulation with IL-23 [138,139], another proinflammatory M1 cytokine [140]. Lee et al provide evidence showing that the inhibition of IL-17 or IL-23 improves wound closure times in diabetic obese mice without impacting scarring or fibrosis [136].…”

Section: Diabetes and Obesitymentioning

confidence: 99%

The Role of IL-6 in Skin Fibrosis and Cutaneous Wound Healing

et al. 2020

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The timely resolution of wound healing is critical for restoring the skin as a protective barrier. The switch from a proinflammatory to a reparative microenvironment must be tightly regulated. Interleukin (IL)-6 is a key modulator of the inflammatory and reparative process: it is involved in the differentiation, activation, and proliferation of leukocytes, endothelial cells, keratinocytes, and fibroblasts. This review examines the role of IL-6 in the healing of cutaneous wounds, and how dysregulation of IL-6 signaling can lead to either fibrosis or a failure to heal. The role of an IL-6/TGF-β feedback loop is discussed in the context of fibrogenesis, while IL-6 expression and responses in advanced age, diabetes, and obesity is outlined regarding the development of chronic wounds. Current research on therapies that modulate IL-6 is explored. Here, we consider IL-6′s diverse impact on cutaneous wound healing.

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Section: Diabetes and Obesitymentioning

confidence: 99%

The Role of IL-6 in Skin Fibrosis and Cutaneous Wound Healing

et al. 2020

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“…IL‐23R plays a pivotal role in the generation and differentiation of pathogenic Th17 cells. IL‐23R mediated signalling requires the binding of its cognate cytokine IL‐23, secreted by macrophages and dendritic cells . IL‐23R leads to activation of STAT3 pathway resulting in functional activation and maturation of Th17 cells .…”

Section: Introductionmentioning

confidence: 99%

Increased interleukin‐23 receptor (IL‐23R) expression is associated with disease severity in acute‐on‐chronic liver failure

Khanam

Trehanpati

Sarin

2019

Liver International

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Abbreviations: ACLF, acute-on-chronic liver failure; CCR6, chemokine receptor 6; CHB, chronic hepatitis B; CTP, Child-Turcotte-Pugh; GM-CSF, granulocyte-macrophage colony-stimulating factor; IL-17R, interleukin-17 receptor; IL-23R, interleukin-23 receptor; IL-, interleukin; INR, international normalized ratio; MELD, Model for End-Stage Liver Disease; ROR-γt, retinoic acid receptor-related orphan nuclear receptor gamma t. AbstractBackground: Th17 cells mediated immune response is important in chronic hepatitis B (CHB) infection and inflammation associated diseases; however, little is known about their immunopathogenic role in acute-on-chronic liver failure (ACLF).Interleukin-23 receptor (IL-23R) is essential for the generation of pathogenic Th17 cells; therefore, we aimed to evaluate IL-23R expression and its correlation with disease severity in ACLF. Methods:Forty-two patients with ACLF (HBV and alcohol-related), thirty-two with CHB and twenty healthy controls (HC) were studied. Circulating and intrahepatic profile of Th17 cells and IL-23R was investigated. Association of IL-23R with disease severity was determined.Results: Circulating Th17 cells were significantly increased in both ACLF groups (P = 0.03, P = 0.006) than CHB and HC. Percentage of Th17 cells was higher in liver than peripheral blood of ACLF patients (P = 0.04). Expression of IL-23R was immensely up-regulated on Th17 cells of ACLF patients. Importantly, IL-23R not only correlated with the increased percentage of Th17 cells but also had significant association with inflammation (P = 0.03) and clinical disease severity indices including Child-Turcotte-Pugh (P = 0.001) and Model for End-Stage Liver Disease (P = 0.002) scores. The ACLF non-survivors showed higher IL-23R expression (P = 0.01).Transcription factor retinoic acid receptor-related orphan nuclear receptor gamma-t (ROR-γt) was also high in circulation and in liver of ACLF patients and it positively correlated with ALT levels (P = 0.03). Surface receptors, including CCR6, IL-17R and pro-inflammatory cytokines IL-17A, IL-22, CXCL8 and GM-CSF were highly augmented in ACLF. Conclusion: ACLF patients express high IL-23R on Th17 cells which induces inflam-mation and strongly correlates with liver disease severity. K E Y W O R D S alcoholic hepatitis, cirrhosis, hepatitis B, IL-17A, IL-23R, liver failure | 1063 KHANAM et Al.

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“…Chen et al, 2019;Sica et al, 2015;Q. Wang et al, 2016;Yamaguchi et al, 2017). The M2 or alternative polarization of macrophages is induced by multiple stimuli such as IL-4, IL-10, and IL-13 and exerts anti-inflammatory responses (da Silva et al, 2015;Luhmann et al, 2016;M.…”

Section: Discussionmentioning

confidence: 99%

Nicotine causes alternative polarization of macrophages via Src‐mediated STAT3 activation: Potential pathobiological implications

Saranyutanon

Acharya

Deshmukh

et al. 2021

Journal Cellular Physiology

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Nicotine is an addictive ingredient of tobacco products and other noncigarette substitutes, including those being used for smoking cessation to relieve withdrawal symptoms. Earlier research, however, has associated nicotine with the risk and poorer outcome of several diseases, including cancer. Macrophages are an important component of the innate immune system and can have both pro-and antiinflammatory functions depending upon their polarization state. Here, we investigated the effect of nicotine on macrophage polarization, growth, and invasion to understand its role in human physiology. We observed that nicotine induced M2 polarization of RAW264.7 and THP-1-derived macrophages in a dose-dependent manner. Cytokine profiling suggested a mixed M2a/d phenotype of nicotinepolarized macrophages associated with tissue repair and pro-angiogenic functions.Moreover, nicotine treatment also enhanced the growth, motility, and invasion of macrophages. Mechanistic studies revealed increased phosphorylation of STAT3 in nicotine-treated macrophages that was mediated through Src activation. Importantly, pretreatment of macrophages with either Src or STAT3 inhibitor abrogated nicotine-induced macrophage polarization, growth, and motility, suggesting a functional role of the Src-STAT3 signaling axis. Together, our findings reveal a novel role of nicotine in immunosuppression via causing M2 polarization of macrophages that could be implicated in the pathogenesis of various diseases.

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Differential regulation of IL-23 production in M1 macrophages by TIR8/SIGIRR through TLR4- or TLR7/8-mediated signaling

Cited by 18 publications

References 28 publications

The Role of IL-6 in Skin Fibrosis and Cutaneous Wound Healing

The Role of IL-6 in Skin Fibrosis and Cutaneous Wound Healing

Increased interleukin‐23 receptor (IL‐23R) expression is associated with disease severity in acute‐on‐chronic liver failure

Nicotine causes alternative polarization of macrophages via Src‐mediated STAT3 activation: Potential pathobiological implications

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