作者: Katharina Ronacher , Roma Sinha , Michelle Cestari
关键词:
摘要: Approximately 10% of individuals latently infected with Mycobacterium tuberculosis (Mtb) develop active (TB) during their lifetime. Although it is well recognized that T-helper 1 immune responses are crucial for containing latent TB infection, the full array host factors conferring protective immunity from progression not completely understood. IL-22 produced by cells innate and adaptive system including lymphoid cells, natural killer as T lymphocytes (Th1, Th17, Th22) binds to its cognate receptor, IL-22R1, which expressed on non-hematopoietic such lung epithelial cells. However, recent studies suggest Mtb induces expression IL-22R1 macrophages multiple have indicated a role in respiratory tract infections. Reduced concentrations circulating compared decreased percentages Mtb-specific producing patients controls designate this cytokine key player immunology. More recently, has been shown type 2 diabetes (T2D) co-morbidity serum further reduced without co-morbidities. whether causative link between low increased susceptibility disease severity exists remains be established. This review summarizes contribution IL-22, potentially under-appreciated resistance TB, at interface response epithelium.