IL-33 accelerates cutaneous wound healing involved in upregulation of alternatively activated macrophages

Yin, Hui; Li, Xiangyong; Hu, Shicheng; Liu, Tao; Yuan, Baohong; Gu, Hong‐Feng; Niu, Qian; Zhang, Xiaofan; Zheng, Fang

doi:10.1016/j.molimm.2013.05.225

Cited by 85 publications

(63 citation statements)

References 39 publications

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“…The percentage of CD206 + macrophages remained high 5 and 7 days after injury, similar to nonwounded skin, and these macrophages were enriched for cytokines and growth factors that promote repair (Figure 1f). These data are consistent with previous studies (Daley et al, 2010; Yin et al, 2013) and indicate that a wound bed macrophage phenotype switch precedes regeneration during the midstage of epidermal and dermal repair.…”

Section: Resultssupporting

confidence: 93%

CD301b+ Macrophages Are Essential for Effective Skin Wound Healing

Shook

Xiao

Kumamoto

et al. 2016

Journal of Investigative Dermatology

115

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Regeneration of skin’s barrier function after injury requires temporally coordinated cellular interactions between multiple cell types. Macrophages are essential inflammatory cells in skin wound regeneration. These cells switch their phenotype from inflammatory in the early regenerative stages to anti-inflammatory in the midstages of healing to coordinate skin repair. However, little is known about how different subsets of anti-inflammatory macrophages contribute to skin wound healing. Here, we characterize midstage macrophages (CD45+/CD11b+/F4-80+) and identify two major populations: CD206+/CD301b+ and CD206+/CD301b−. The numbers of CD206+/CD301b+ macrophages increased concomitantly with repair, when the anti-inflammatory phenotype switch occurs in midstage healing. Using diphtheria toxin–mediated depletion models in mice, we show that selective depletion of midstage CD301b-expressing macrophages phenocopied wound healing defects observed in mice where multiple myeloid lineages are depleted. Additionally, when FACS-isolated subpopulations of myeloid cells were transplanted into 3-day wounds of syngeneic mice, only CD206+/CD301b+ macrophages significantly increased proliferation and fibroblast repopulation. These data show that the CD301b-expressing subpopulation of macrophages is critical for activation of reparative processes during the midstage of cutaneous repair.

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Section: Resultssupporting

confidence: 93%

CD301b+ Macrophages Are Essential for Effective Skin Wound Healing

Shook

Xiao

Kumamoto

et al. 2016

Journal of Investigative Dermatology

115

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“…13 Complementing the beneficial role of IL-33, additional studies have indicated that a faster healing process is seen when mice bearing skin wounds are treated with this cytokine, due to an increase in collagen deposition, which allows a better re-epithelialization of the tissue. 14 This last observation is of great importance for the transplantation field, where a correct healing of the injured tissue is necessary for the appropriate function of the new organ.…”

Section: M M U N O L O G Y O R I G I N a L A R T I C L Ementioning

confidence: 99%

Exogenous interleukin‐33 targets myeloid‐derived suppressor cells and generates periphery‐induced Foxp3⁺ regulatory T cells in skin‐transplanted mice

et al. 2015

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SummaryInterleukin-33 (IL-33) has been a focus of study because of its variety of functions shaping CD4 + T-cell biology. In the present work, we evaluated the modulatory effect of IL-33 on suppressor cells in an in vivo transplantation model. C57BL/6 wild-type mice were grafted with syngeneic or allogeneic skin transplants and treated with exogenous IL-33 daily. After 10 days of treatment, we analysed draining lymph node cellularity and found in allogeneic animals an increment in myeloid-derived suppressor cells, which co-express MHC-II, and become enriched upon IL-33 treatment. In line with this observation, inducible nitric oxide synthase and arginase 1 expression were also increased in allogeneic animals upon IL-33 administration. In addition, IL-33 treatment up-regulated the number of favours an anti-inflammatory or tolerogenic state by skewing cytokine production. Therefore, our data suggest a potential use of IL-33 to prevent allograft rejection, bringing new therapeutics to the transplantation field.

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“…In order to explore whether these may play a functional role in wound healing in organs other than the intestine, they investigated the role of these in a rat skin wound healing assay. [54]. Although it seems from these reports that IL-33 signalling at the site of cutaneous damage may facilitate the transition of macrophages from a pro-inflammatory to a prorepair phenotype thereby promoting dermal wound healing, the underlying mechanism for IL-33 in skin wound healing remains unclear.…”

Section: Il-33 In Cutaneous Wound Healingmentioning

confidence: 99%

Wounds that heal and wounds that don’t − The role of the IL-33/ST2 pathway in tissue repair and tumorigenesis

Millar

O'Donnell

McInnes

et al. 2017

Seminars in Cell & Developmental Biology

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IL-33 accelerates cutaneous wound healing involved in upregulation of alternatively activated macrophages

Cited by 85 publications

References 39 publications

CD301b+ Macrophages Are Essential for Effective Skin Wound Healing

CD301b+ Macrophages Are Essential for Effective Skin Wound Healing

Exogenous interleukin‐33 targets myeloid‐derived suppressor cells and generates periphery‐induced Foxp3⁺ regulatory T cells in skin‐transplanted mice

Wounds that heal and wounds that don’t − The role of the IL-33/ST2 pathway in tissue repair and tumorigenesis

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IL-33 accelerates cutaneous wound healing involved in upregulation of alternatively activated macrophages

Cited by 85 publications

References 39 publications

CD301b+ Macrophages Are Essential for Effective Skin Wound Healing

CD301b+ Macrophages Are Essential for Effective Skin Wound Healing

Exogenous interleukin‐33 targets myeloid‐derived suppressor cells and generates periphery‐induced Foxp3+ regulatory T cells in skin‐transplanted mice

Wounds that heal and wounds that don’t − The role of the IL-33/ST2 pathway in tissue repair and tumorigenesis

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Exogenous interleukin‐33 targets myeloid‐derived suppressor cells and generates periphery‐induced Foxp3⁺ regulatory T cells in skin‐transplanted mice