肺滞在型メモリーCD8T細胞長期維持法の開発

Although tissue-resident memory CD8 T cells (CD8 TRMs) in the lung mucosa confer localized protection against challenges with various strains of influenza viruses, their longevity is shorter than that of other tissues. In this study, we aimed to elucidate the differentiation and maintenance mechanisms of pulmonary CD8 TRMs in order to extend their longevity. First, we found that pulmonary macrophages promote TRM differentiation by providing local antigen stimulation in the early stages of infection. We also found that the lung CD8 TRM is maintained in an autophagy-independent manner even during starvation. We also found that when long-term antigen presentation is induced following intranasal immunization with adenovirus vectors. As a result, circulating memory T cells are continuously activated and differentiate into TRM in the lung. Understanding the mechanisms by which prolonged antigen presentation would help in the development of vaccination strategies to generate long-lived TRM.