Do not be alarmed: understanding <scp>IL</scp>33‐<scp>ST</scp>2 signalling in wound repair

Ansell, David M.; Hardman, Matthew J.

doi:10.1111/exd.12887

Cited by 3 publications

(3 citation statements)

References 9 publications

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“…Both TSLP and IL‐33 were proposed to function as alarmins that alert the immune system and spur a Th2 immune response following tissue damage. 49 , 51 , 52 Moreover, IL‐33 can exert immunosuppressive functions by induction of T‐regs after barrier impairment, thereby preventing exaggerated skin inflammation. 50 Furthermore, IL‐33 and TSLP were suggested to directly dampen epidermal barrier function by downregulation of FLG expression.…”

Section: Discussionmentioning

confidence: 99%

“…Additionally, we report decreased mRNA expression levels of both cytokines 24 h after milder epidermal barrier perturbation, in absence of the earlier (6 h) upregulation (Figure 2B). Both TSLP and IL‐33 were proposed to function as alarmins that alert the immune system and spur a Th2 immune response following tissue damage 49,51,52 . Moreover, IL‐33 can exert immunosuppressive functions by induction of T‐regs after barrier impairment, thereby preventing exaggerated skin inflammation 50 .…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Keratinocyte‐derived IL‐1β induces PPARG downregulation and PPARD upregulation in human reconstructed epidermis following barrier impairment

Blunder

Krimbacher

Moosbrugger‐Martinz

et al. 2021

Experimental Dermatology

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Keratinocyte‐derived IL‐1β induces PPARG downregulation and PPARD upregulation in human reconstructed epidermis following barrier impairment

Blunder

Krimbacher

Moosbrugger‐Martinz

et al. 2021

Experimental Dermatology

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“…Increased IL-33 expression was found in wound tissue, and exogenous IL-33 can promote the deposition of collagen and fibronectin to enhance wound healing (Yin et al, 2013). In addition to direct wound healing effects, an accumulation of evidence indicates that ILC2s constitutively express ST2 and respond rapidly to IL-33, which can be an important regulator for restoring epithelial integrity and tissue homeostasis to close the wound (Ansell and Hardman, 2016). After IL-33 stimulation, ILC2s expressing ST2 contribute to reepithelialization, in part through the secretion of the epidermal growth factor amphiregulin in skin lesions of atopic dermatitis (Salimi et al, 2013).…”

Section: Discussionmentioning

confidence: 99%

Increased Type 2 Innate Lymphoid Cells in Patients with Drug Reaction with Eosinophilia and Systemic Symptoms Syndrome

Tsai

Liou

Hung³

et al. 2019

Journal of Investigative Dermatology

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Drug reaction with eosinophilia and systemic symptoms (DRESS) syndrome is a life-threatening disorder with an estimated mortality rate of 2%. Recently, type II innate lymphoid cells (ILC2s) have been implicated as an important contributor to the pathogenesis of allergic disorders. However, the roles of ILC2s and ILC2associated cytokines in DRESS remain unclear. Herein, we enrolled 54 participants (including 24 patients with DRESS syndrome and 30 healthy controls), and identified the increased ST2 þ ILC2s population in skin lesions/blood. In addition, serum soluble ST2 (sST2), IL-5, and TSLP levels were significantly elevated at the acute stage of patients with DRESS. Decreased ILC2s population, serum sST2, and IL-5, accompanied with rash, eosinophilia, and alanine aminotransferase improvement were observed after steroid treatment. In the delayed-responders group (n ¼ 13), serum IL-33, sST2, IL-5, and TSLP levels were significantly increased at the acute phase, but only sST2 levels correlated with alanine aminotransferase and eosinophil improvement at the 4-week follow-up visit. Serum sST2 levels were also correlated with IL-33 (r ¼ 0.49; P ¼ 0.02) and alanine aminotransferase levels (r ¼ 0.65; P < 0.01) at the onset of DRESS. Our results demonstrated high IL-33/ST2 expression in ILC2 cells plays a role in skin inflammation of drug hypersensitivity, and serum sST2 levels can be as a potential biomarker to predict liver involvement in patients with DRESS syndrome.

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Interleukin‐33 encourages scar formation in murine fetal skin wounds

Wulff

Pappa

Wilgus

2018

Wound Repair Regeneration

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The magnitude of the inflammatory response after skin injury is important for determining whether wounds in developing fetal skin will heal scarlessly (minimal inflammation) or with prominent scars (robust inflammation). One class of inflammatory mediators gaining attention for their role in wound inflammation is alarmins. In the current study, the alarmin IL-33 was examined in a mouse model of fetal wound healing. IL-33 expression was elevated in scar-forming embryonic day 18 wounds compared to scarless embryonic day 15 wounds. Furthermore, injection of IL-33 into embryonic day 15 wounds caused scarring when wounds were analyzed at 7 days post-wounding. The introduction of IL-33 into embryonic day 15 wounds did not induce statistically significant changes in the number of neutrophils, mast cells, or macrophages in vivo. However, IL-33 treatment enhanced collagen expression in cultured fibroblasts derived from adult and fetal murine skin, suggesting that IL-33 may directly stimulate fibroblasts. In vitro studies suggested that the stimulation of collagen production by IL-33 in fibroblasts was partially dependent on NF-κB activation. Overall, the data suggest an association between IL-33 and scar formation in fetal wounds.

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Do not be alarmed: understanding IL33‐ST2 signalling in wound repair

Cited by 3 publications

References 9 publications

Keratinocyte‐derived IL‐1β induces PPARG downregulation and PPARD upregulation in human reconstructed epidermis following barrier impairment

Keratinocyte‐derived IL‐1β induces PPARG downregulation and PPARD upregulation in human reconstructed epidermis following barrier impairment

Increased Type 2 Innate Lymphoid Cells in Patients with Drug Reaction with Eosinophilia and Systemic Symptoms Syndrome

Interleukin‐33 encourages scar formation in murine fetal skin wounds

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