Professor Akira Shibuya, Assistant Professor Chigusa Oda, and others at the Center for Survival Research, University of Tsukuba, have found that dead cells in the mucous membranes of the intestinal tract, skin, and trachea stimulate immune cells to cause inflammatory bowel disease, atopic dermatitis, and asthma. It was discovered that it promotes the onset of.The development of new treatments for these diseases is expected.
Mucous membranes such as the intestine, skin, and trachea are protected by epithelial cells, which maintain the mucous membrane by constantly repeating death and renewal.Dead cells are excreted as dirt, feces, sputum, etc., and have been said to have no particular role.The research group discovered a protein molecule called CD2003a in immune cells in 300, and in 2012, when CD300a binds to a phospholipid called phosphatidylserine expressed from dead cells, it suppresses the activation of immune cells. Confirming.This time, we found that it is immune cells called dendritic cells and Langerhans cells that express CD300a, and that these immune cells are attached to dead epithelial cells.Furthermore, it was found that when CD300a binds to dead cell phosphatidylserine, it regulates the number of regulatory T cells in mucosal cell tissue.When immune cells are activated, they exacerbate enteritis, atopic dermatitis, and asthma, but regulatory T cells have the function of suppressing the activation of immune cells.This study revealed that dead cells in the mucosal epithelium reduce the number of regulatory T cells in mucosal tissues such as the intestine, skin, and trachea via CD300a and are involved in the promotion of disease.
The number of patients with inflammatory bowel disease (ulcerative colitis, Crohn's disease) and allergic diseases (asthma, atopic dermatitis, etc.), which are intractable diseases of unknown cause, is increasing year by year.Based on the role of dead cells in the mucous membrane revealed by this study, it is possible to bring about innovative treatment by developing a new drug that suppresses the action of CD300a.