Epithelial surfaces represent an important interface between the body and the environment. They are continuously exposed to environmental stimuli and contribute to homeostasis. Upon environmental stress challenges such as wounding or cancer, epithelia undergo an extensive reorganization of immunity to repair the injured or transformed site. Specifically, DETCs, a γδ T cell subpopulation, preferentially located in skin epithelia, provide essential functions for skin wound healing through multiple mechanisms.

When keratinocytes are injured, they stimulate the TCR of DETC. Costimulatory signals are provided to DETC by junctional adhesion molecule-like protein (JAML) with Coxsackie and Adenovirus Receptor (CAR) on wounded keratinocytes. When activated, DETCs secrete factors such as keratinocyte growth factors (KGFs) which aid wound healing and release inflammatory cytokines (e.g. IFN-γ , IL-2, TNF-α) and chemokines (e.g. CCL3, CCL4, CCL5) to recruit cells into the damage site. Recently, DETCs have also been found to contribute to cancer immunosurveillance. Tumor cell surface NKG2D molecules trigger TCRs of DETCs, and activate anti-tumor molecule (e.g. IFN-γ) expression. However, the mechanistic details of the DETC response in both wound healing and tumor immunity are largely unknown.

A standard EDITORIAL TRACKING SYSTEM is utilized for manuscript submission, review, editorial processing and tracking which can be securely accessed by the authors, reviewers and editors for monitoring and tracking the article processing. Manuscripts can be uploaded online at Editorial Tracking System (https://www.longdom.org/submissions/hair-therapy-transplantation.html) or forwarded to the Editorial Office at hairtherapy@emedscholar.com

Media Contact:               

Sandra Jones

Journal Manager

Hair Therapy and Transplantation

Email: hairtherapy@emedscholar.com