胸腺基质淋巴细胞生成素控制毛发生长。
Thymic stromal lymphopoietin controls hair growth.
机构信息
Department of Dermatology, Duke University, P.O. Box 103052, Durham, NC 27710, USA; Department of Immunology, Duke University, Durham, NC 27710, USA.
Genomic and Computational Biology, Duke University, Durham, NC 27705, USA.
出版信息
Stem Cell Reports. 2022 Mar 8;17(3):649-663. doi: 10.1016/j.stemcr.2022.01.017. Epub 2022 Feb 24.
Skin tissue regeneration after injury involves the production and integration of signals by stem cells residing in hair follicles (HFSCs). Much remains unknown about how specific wound-derived factors modulate stem cell contribution to hair growth. We demonstrate that thymic stromal lymphopoietin (TSLP) is produced in response to skin injury and during the anagen phase of the hair cycle. Intradermal injection of TSLP promoted wound-induced hair growth (WIHG), whereas neutralizing TSLP receptor (TSLPR) inhibited WIHG. Using flow cytometry and fluorescent immunostaining, we found that TSLP promoted proliferation of transit-amplifying cells. Lgr5-mediated deletion of Tslpr in HFSCs inhibited both wound-induced and exogenous TSLP-induced hair growth. Our data highlight a novel function for TSLP in regulation of hair follicle activity during homeostasis and wound healing.
皮肤损伤后的组织再生涉及毛囊干细胞（HFSCs）产生和整合信号。目前尚不清楚特定的伤口来源因子如何调节干细胞对毛发生长的贡献。我们证明胸腺基质淋巴细胞生成素（TSLP）是对皮肤损伤和毛发周期的生长期做出响应而产生的。TSLP 的皮内注射促进了创伤诱导的毛发生长（WIHG），而中和 TSLP 受体（TSLPR）则抑制了 WIHG。通过流式细胞术和荧光免疫染色，我们发现 TSLP 促进了过渡扩增细胞的增殖。HFSCs 中 Lgr5 介导的 Tslpr 缺失抑制了创伤诱导和外源性 TSLP 诱导的毛发生长。我们的数据强调了 TSLP 在调节静止期和创伤愈合过程中毛囊活性方面的新功能。
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