Chronic inflammation contributes to the development of a variety of diseases, including immunological diseases such as allergies and autoimmune diseases, as well as neurodegenerative, cardiovascular, and metabolic diseases, and even cancer and aging. Therefore, many examples prove that controlling chronic inflammation improves the pathological condition. In practice, however, treatment options for many intractable diseases are limited, leaving significant unmet needs. 
Immune cells, particularly innate immune cells such as macrophages and neutrophils, play a central role in chronic inflammation. These cells mediate both inflammation and tissue repair. The regulation of innate immune cell functions, including functional remodeling (i.e. functional plasticity: either inflammatory or reparative), remains enigmatic. 
Innate immune cells detect various inflammatory substances, such as pathogens and dead cells, and transmit inflammatory signals into cells. These signals are then integrated with metabolic signals in endolysosomes, converting them into cellular responses. In this way, endolysosomes function as hubs that relay and integrate complex, diverse signals during inflammatory responses. Consequently, interrupting the acidification of endolysosomes and disrupting their function in innate immune cells is an effective method of reducing inflammation and, in some cases, inducing tissue repair. This implies that endolysosomes are crucial for the functional plasticity of innate immune cells. Our focus is on the endolysosomal system, which plays a key role in the functional plasticity of innate immune cells. Our goal is to identify new therapeutic targets for intractable diseases by clarifying how innate immune cells acquire proinflammatory or tissue-repair abilities. This will pave the way for academic drug discovery. We welcome students and colleagues interested in conducting basic research that can be translated into social applications.