T-Regulating Hair Follicle Stem Cells
Regulatory T (Treg) cells are key regulators of immune tolerance and are capable of suppressing multiple immune cell types and blocking excessive inflammatory responses. Although roles for tissue-resident Foxp3+ Treg cells in maintaining non-lymphoid tissue homeostasis have been suggested, evidence of a relationship between tissue-specific stem cells and Treg cells remains sparse
Regulatory T (Treg) cells are key regulators of immune tolerance and are capable of suppressing multiple immune cell types and blocking excessive inflammatory responses. Although roles for tissue-resident Foxp3+ Treg cells in maintaining non-lymphoid tissue homeostasis have been suggested, evidence of a relationship between tissue-specific stem cells and Treg cells remains sparse. In a recent issue of Cell, Ali et al., (2017) report a function for skin-resident subsets of Treg cells in regulating the proliferation and differentiation of hair follicle stem cells (HFSCs) by activating the Jag1-Notch signaling pathway, thereby suggesting a direct relationship between stem cells and resident immune cells.
Human and murine Treg cells, identified among CD4+CD25+ T cells by the expression of the transcription factor forkhead box P3 (Foxp3), can induce immune suppression by the production of inhibitory cytokines, cytolysis of effector cells, metabolic disruption, and modulation of dendritic cell function.
Tissue-resident Treg cells, unlike those residing in primary and secondary lymphoid organs, hold unique functional capacities specific to their tissue of origin. In visceral adipose tissues, Treg cells regulate lipid and glucose metabolism via peroxisome proliferator-activated receptor g (Pparg) signaling. In muscle and lung tissues, Treg cells expressing amphiregulin, an epidermal growth factor receptor ligand, appear to be critical for tissue regeneration and wound healing. An interesting connection between Treg cells and stem cells has been established in the hematopoietic system, where Treg cells can form immune-privileged sites to generate a protective niche for hematopoietic stemcells (HSCs).
Reference: http://www.cell.com/immunity/fulltext/S1074-7613(17)30239-X
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