A group of Assistant Professor Yuki Morimoto, Associate Professor Kiyoshi Hirahara, and Professor Toshinori Nakayama of the Graduate School of Medicine, Chiba University identified a new cell population that induces tissue fibrosis that occurs in severe asthma, and new tissue fibrosis. The mechanism was clarified.
Currently, inhaled steroids are generally used to treat bronchial asthma, which is a severe allergic disease, but steroids are ineffective for tissue fibrosis that has once occurred, and new treatments are required. ing.Tissue fibrosis causes shortness of breath and dyspnea, which significantly reduces the QOL of affected patients, but the molecular mechanism by which fibrosis occurs has been unclear.
This time, the research group investigated the mechanism of inducing fibrosis around the airways and identified "fibrosis-inducing-pathogenic memory T cells" that specifically produce a protein called Amphiregulin. Amphiregulin is a type of white blood cell that stimulates eosinophils, which are deeply involved in the onset of asthma.The stimulated eosinophils secrete the fibrosis-causing protein "Osteopontin", which directly causes tissue fibrosis.The group also found that suppressing the action of EGF receptors expressed on eosinophils suppressed tissue fibrosis caused by the Amphiregulin-Osteopontin pathway.
With this result, the Amphiregulin-Osteopontin pathway is expected to be a target for breakthrough therapeutic agents for asthma, and EGF receptor inhibitors are already widely used as therapeutic agents for lung cancer. , The possibility of drug repositioning is also expected.
Paper information:[Immunity] Amphiregulin-producing pathogenic memory T helper-2 cells instruct eosinophils to secrete Osteopontin and facilitate airway fibrosis