On February 17, 2015, researchers at Huimin Zhang’s group published an article entitled “Structural Damage in the C. elegans Epidermis Causes Release of STA-2 and Induction of an Innate Immune Response” in Immunity. This work was selected as the “Free featured article” of the issue and previewed by Dr. Irazoqui of Harward Medical School.
The epidermis constantly encounters invasions that disrupt its architecture, yetwhether the epidermal immune system utilizes damaged structures as danger signals to activate self-defense is unclear. Here, we used a C. elegans epidermis model in which skinpenetrating infection or injury activates immune defense and antimicrobial peptide (AMP) production. By systemically disrupting each architectural component, we found that only disturbance of the apical hemidesmosomes triggered an immune response and robust AMP expression. The epidermis recognized structural damage through hemidesmosomes associated with a STAT-like protein, whose disruption led to detachment of STA-2 molecules from hemidesmosomes and transcription of AMPs. This machinery enabled the epidermis to bypass certain signaling amplification and directly trigger AMP production when subjected to extensive architectural damage. Together, our findings uncover an evolutionarily conserved mechanism for the epithelial barriers to detect danger and activate immune defense.
Yun Zhang is the first authors of the paper. Contributing authors include Wenna Li,Linfeng Li,Yuanbao Li,Rong Fu,Yi Zhu,Jie Li andYanfeng Zhou. Prof. Sidong Xiong and Prof Huimin Zhang are the corresponding authors of the paper. This work has been supported by grants from Major State Basic Research Development Program of China (2013CB530501), National Natural Science Foundation of China (31271429 and 31471265), Jiangsu Provincial Innovative Research Team, the Program for Changjiang Scholars and Innovative Research Team in University, and the Priority Academic Development Program of Jiangsu Province Higher Education Institutions.