Current influenza vaccines target mutated viral surface proteins and are therefore only effective against certain types of viruses.In addition, the infection itself cannot be prevented because the effect of inducing an immune response cannot be expected in the respiratory mucosa, which is the gateway to viral entry.On the other hand, CD8-positive T cells (a type of lymphocyte) can directly destroy virus-infected cells by targeting viral proteins with few mutations, so if CD1-positive T cells can be deployed at the site of infection, all types of influenza virus infection can occur. A quick end is possible.In recent years, it has become clear that there are cells (stay-type memory T cells) that are maintained in the infected area near the invasion gate for a long period of time and are responsible for protective immunity against reinfection.If the stay-type CD8-positive memory T cells can be effectively induced and maintained at the entry gate, it will lead to the development of an influenza virus vaccine that is effective against multiple strains and has a high protective effect.

　Takamura et al., The stay-type CD8-positive memory T cells present in the lungs of virus-infected mice are localized in cell clumps formed to repair damage to lung tissue caused by infection, and are the most secondary infections. Found to protect a dangerous "wound" and named this agglomerate "repair-related memory storage site" (RAMD).We also found that viral antigens need to remain locally in order to maintain staying CD8-positive memory T cells in RAMD.

　In the future, if the details of the RAMD formation mechanism and the locally staying CD8-positive memory T cell differentiation induction mechanism are elucidated, it is expected to develop a vaccine that enables a wide range of protective immunity.