About this Research Topic
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.
This Research Topic will summarize the current understanding of DETC functions in wound healing and cancer, with underlying molecular mechanisms. Moreover, it will also further address the interactions between DETCs and neighboring cells (e.g. keratinocytes and immune cells), which are important for successful wound repair and cancer immune surveillance. We welcome authors to submit Review and Original research articles focusing on, but not limited to, the following subtopics:
1. DETCs signaling pathways including new sensors, activation mechanisms, and effector molecules
2. Interaction between DETCs and neighboring cells
3. New therapies targeting DETCs for epithelial injury and cancer
Topic Editor Prof. Zhinan Yin is the co-founder of JIDEI Kongming Biotech. All other Topic Editors declare no competing interests with regards to the Research Topic subject
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.
This Research Topic will summarize the current understanding of DETC functions in wound healing and cancer, with underlying molecular mechanisms. Moreover, it will also further address the interactions between DETCs and neighboring cells (e.g. keratinocytes and immune cells), which are important for successful wound repair and cancer immune surveillance. We welcome authors to submit Review and Original research articles focusing on, but not limited to, the following subtopics:
1. DETCs signaling pathways including new sensors, activation mechanisms, and effector molecules
2. Interaction between DETCs and neighboring cells
3. New therapies targeting DETCs for epithelial injury and cancer
Topic Editor Prof. Zhinan Yin is the co-founder of JIDEI Kongming Biotech. All other Topic Editors declare no competing interests with regards to the Research Topic subject
Keywords: DETCs, Wound Healing, Cancer Immunology, Inflammation, keratinocytes
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