Functions of Vγ4 T Cells and Dendritic Epidermal T Cells on Skin Wound Healing

Li, Yashu; Wu, Jun; Luo, Gaoxing; Wang, He

doi:10.3389/fimmu.2018.01099

Cited by 47 publications

(42 citation statements)

References 79 publications

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“…However, at early time points after infection, dermal  T cells likely moderate wound healing, at least partially, via production of IL-17A in response to cutaneous VACV infection.  T cells have long been known to play a role in cutaneous wound healing after activation by KCs [30][31][32][33], where they migrate to a site of injury [26,34,35] and produce of a number of cytokines that promote the wound healing response [36][37][38][39][40][41][42][43][44]. We did find a marked increase in VACVinduced pathology in the absence of  T cells, consistent with a role for these cells in establishment of the wound healing response following VACV infection.…”

Section: Discussionsupporting

confidence: 81%

“…In various skin pathologies  T cell subsets each have distinct functions, including production of IFN- [17][18][19][20][21] or IL-17A [22][23][24][25], recruitment of myeloid cells [26,27], lysis of virus infected cells [18,28,29] and pro-wound healing functions [26,[30][31][32][33][34][35][36][37][38][39][40][41][42][43][44]. Therefore, it is likely that each resident  T cell type, along with recruited  T cells, has a differential ability to be activated, and correspondingly, a different function, following cutaneous VACV infection.…”

Section: Introductionmentioning

confidence: 99%

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γδ T cells mediate a requisite portion of a wound healing response triggered by cutaneous poxvirus infection

Reider

Lin

Krouse

et al. 2020

Preprint

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Infection at peripheral sites, such as the skin, activates local innate immune defenses tasked with limiting spread of the pathogen while preserving tissue integrity. T cells bearing γδ T Cell Receptors (TCR), which comprise multiple phenotypically distinct subtypes of cells, reside in normal skin, where they shape immunity to cutaneous infection, prior to onset of an adaptive immune response by conventional αβ CD4+ (TCD4+) and CD8+ (TCD8+) T cells. The mechanisms used by γδ T cells to control virus replication and tissue pathology following cutaneous infection are unknown, so we examined the role of γδ T cells in the response to cutaneous infection with vaccinia virus (VACV). Resident γδ T cells in the skin expanded and combined with recruited γδ T cells to control the pathology observed after cutaneous VACV infection. However, we observed no defect in control of local virus replication or increased systemic spread in mice lacking γδ T cells, despite induction of a cytolytic response in a specialized subset of resident γδ T cells. While examining γδ T cell-mediated control of tissue pathology following cutaneous VACV infection, we identified a unique wound healing signature associated with cutaneous virus infection that has features that are common to, but also features that antagonize, the sterile cutaneous wound healing response. Typically, tissue repair is thought to occur only after clearance of a pathogen, but the viral wound healing signature was evident prior to the peak of virus replication in the skin. Resident and recruited γδ T cells contributed to this wound healing signature through induction of multiple cytokines and growth factors required for efficient wound closure. Therefore, γδ T cells are early mediators of the wound healing response following cutaneous virus infection and are likely important in maintenance of skin barrier function and prevention of secondary bacterial infection.Author Summaryγδ T cells resident in the skin are among the first immune cell types positioned to be able to respond to a virus infection of the skin. Therefore, it was assumed that these cells in the skin play a role similar to their role after widespread infection throughout the body, namely to kill virus infected cells and slow virus replication and spread. However, we found no role for γδ T cells in control of virus replication after infection of the skin. Rather, the γδ T cells functioned as a critical component of a previously unrecognized wound healing response that is started early after virus infection of the skin, and occurs at the same time as the immune response that aims to clear the virus. This study is the first to describe both the early wound healing response after virus infection, and the role of γδ T cells in that response, and this information could allow manipulation of this response to decrease secondary bacterial infection and change scarring after virus skin infections.

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Section: Discussionsupporting

confidence: 81%

Section: Introductionmentioning

confidence: 99%

γδ T cells mediate a requisite portion of a wound healing response triggered by cutaneous poxvirus infection

Reider

Lin

Krouse

et al. 2020

Preprint

View full text Add to dashboard Cite

show abstract

“…Interleukin-17 activates many signaling cascades and production of another cytokines such as IL-6, TNF-α, and IL-1β (Li, Wu, Luo, & He, 2018). IL-17 is also involved in the induction of pro-inflammatory responses (Akitsu & Iwakura, 2018).…”

Section: Discussionmentioning

confidence: 99%

Evaluation of keratin biomaterial containing silver nanoparticles as a potential wound dressing in full‐thickness skin wound model in diabetic mice

Konop

Czuwara

Kłodzińska

et al. 2020

J Tissue Eng Regen Med

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Keratin is a cytoskeletal scaffolding protein essential for wound healing and tissue recovery. The aim of the study was to evaluate the potential role of insoluble fur keratin‐derived powder containing silver nanoparticles (FKDP‐AgNP) in the allogenic full‐thickness surgical skin wound model in diabetic mice. The scanning electron microscopy image evidenced that the keratin surface is covered by a single layer of silver nanoparticles. Data obtained from dynamic light scattering and micellar electrokinetic chromatography showed three fractions of silver nanoparticles with an average diameter of 130, 22.5, and 5 nm. Microbiologic results revealed that the designed insoluble FKDP‐AgNP dressing to some extent inhibit the growth of Escherichia coli and Staphylococcus aureus. In vitro assays showed that the FKDP‐AgNP dressing did not inhibit fibroblast growth or induce hemolysis. In vivo studies using a diabetic mice model confirmed biocompatible properties of the insoluble keratin dressings. FKDP‐AgNP significantly accelerated wound closure and epithelization at Days 5 and 8 (p < .05) when compared with controls. Histological examination of the inflammatory response documented that FKDP‐AgNP‐treated wounds contained predominantly macrophages, whereas their untreated variants showed mixed cell infiltrates rich in neutrophils. Wound inflammatory response based on macrophages favors tissue remodeling and healing. In conclusion, the investigated FKDP‐AgNP dressing consisting of an insoluble fraction of keratin, which is biocompatible, significantly accelerated wound healing in a diabetic mouse model.

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“…Moreover, GLSO reduced IL-17A and IFN-γ expression after skin injury. IL-17A was reported to impair skin wound closure, while IFN-γ could decrease collagen formation and angiogenesis in wound healing [ 38 – 40 ]. Therefore, GLSO was able to accelerate skin wound healing by possibly regulating the relative levels of inflammatory cytokines.…”

Section: Discussionmentioning

confidence: 99%

The effect of Ganoderma lucidum spore oil in early skin wound healing: interactions of skin microbiota and inflammation

Jiao

Xie

Huang³

et al. 2020

Aging

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The mushroom Ganoderma lucidum (G. lucidum Leyss. ex Fr.) Karst has been a traditional Chinese medicine for millennia. In this study, we isolated the Ganoderma lucidum spore oil (GLSO) and evaluated the effect of GLSO on skin burn wound healing and the underlying mechanisms. Mice were used to perform skin wound healing assay. Wound analysis was performed by photography, hematoxylin/eosin staining, Masson’s Trichrome staining and immunohistochemical analysis. Microbiota on the wounds were analyzed using the 16s rRNA sequence and quantitative statistics. The lipopolysaccharide (LPS) content was examined in skin wounds and serum using an enzyme-linked immunosorbent assay (ELISA). The expression of Toll-like receptor 4 (TLR4) and the relative levels of inflammatory cytokines were determined by qPCR and immunofluorescence assay. A pseudo-germfree mouse model treated with antibiotics was used to investigate whether GLSO accelerated skin burn wound healing through the skin microbiota. We found that GLSO significantly accelerated the process of skin wound healing and regulated the levels of gram-negative and gram-positive bacteria. Furthermore, GLSO reduced LPS and TLR4, and levels of some other related inflammatory cytokines. The assay with the pseudo-germfree mice model showed that GLSO had a significant acceleration on skin wound healing in comparison with antibiotic treatment. Thus, GLSO downregulated the inflammation by regulating skin microbiota to accelerate skin wound healing. These findings provide a scientific rationale for the potential therapeutic use of GLSO in skin burn injury.

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Functions of Vγ4 T Cells and Dendritic Epidermal T Cells on Skin Wound Healing

Cited by 47 publications

References 79 publications

γδ T cells mediate a requisite portion of a wound healing response triggered by cutaneous poxvirus infection

γδ T cells mediate a requisite portion of a wound healing response triggered by cutaneous poxvirus infection

Evaluation of keratin biomaterial containing silver nanoparticles as a potential wound dressing in full‐thickness skin wound model in diabetic mice

The effect of Ganoderma lucidum spore oil in early skin wound healing: interactions of skin microbiota and inflammation

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