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Boothby, I. C., Cohen, J. N., & Rosenblum, M. D. (2020). Regulatory T cells in Skin Injury: At the Crossroads of Tolerance and Tissue Repair. Science Immunology, 5(47), eaaz9631. 
Added by: Dr. Enrique Feoli (01/09/2025, 01:30)   Last edited by: Dr. Enrique Feoli (01/09/2025, 01:48)
Resource type: Journal Article
DOI: 10.1126/sciimmunol.aaz9631
ID no. (ISBN etc.): 2470-9468
BibTeX citation key: Boothby2020
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 Categories: BioAcyl Corp
Subcategories: Disease Tolerance
Creators: Boothby, Cohen, Rosenblum
Collection: Science Immunology		 Views: 3/19
Abstract
Skin injury is a highly inflammatory process that is carefully regulated to mitigate tissue damage and allow for proper barrier repair. Regulatory T cells (Tregs) are crucial coordinators of the immune response to injury in several organs. Here, we review the emerging role of Tregs in facilitating skin repair after injury. We focus on recently discovered interactions between lymphocytes and nonhematopoietic cells during wound healing and discuss how these interactions are regulated both by “classical” suppressive mechanisms of Tregs and by “nonclassical” reparative Treg functions., This review summarizes the recent advances in our understanding of the roles of regulatory T cells in skin injury and tissue repair.
  
Notes

Participation of Type 2 and Type 3 Lymphocytes in Cutaneous Tissue Repair

Left: The type 2 immune response to skin injury is triggered by release of alarmins such as TSLP, IL-18, and IL-33 from damaged keratinocytes, endothelial cells, and stromal cells. Locally resident type 2 lymphocytes such as ILC2s sense these tissue damage signals and produce IL-4, IL-13, and amphiregulin in response. These cytokines promote wound closure by activating wound-contracting myofibroblasts, both directly by signaling to nearby fibroblasts and indirectly by inducing alternative activation of macrophages (AAM). Type 2 cytokines are also capable of driving keratinocyte proliferation and therefore may promote re-epithelialization.

Right: Type 3 lymphocytes are abundant in skin and respond to both microbial ligands and tissue damage signals released by keratinocytes and myeloid cells, including IL-1β and IL-23. IL-17 and IL-22 produced by these cells act directly on keratinocytes, resulting in a two-pronged tissue protective response. First, antimicrobial immunity is bolstered by neutrophil recruitment and antimicrobial peptide production. Secondly, these cytokines reinforce the epidermal barrier by driving keratinocyte proliferation to cover injury sites at the expense of keratinocyte maturation.

Solid arrows, known interactions; Dotted arrows, likely interactions based on data from other tissues and contexts.

 


  
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