Abstract
Immunological memory has a central role in the adaptive immune systems that can efficiently eliminate pathogens such as virus and bacteria. Particularly, memory CD4 T cells function as a control tower of the adaptive immune systems. However, memory helper T (Th) cells are also involved in the pathogenesis of various chronic inflammatory diseases, including asthma. Recently, we have found IL-5-producing pathogenic population in memory Th2 cells in allergic asthma. We term this population memory-type ‘pathogenic Th2 cells (Tpath2 cells)’ in the airway. Several groups also reported distinct memory type Th2 populations, which produce a large amount of IL-5 or multiple cytokines in addition to IL-4 and IL-13. These populations seem to be responsible for the pathology of chronic inflammatory disorders. Our recent study has revealed that ST2 (a component of IL-33 receptor) expression on Tpath2 cells plays an important role for inducing pathogenicity in memory Th2 cells. Here, we highlight the regulation and function of IL-33 and ST2 on memory Th2 cells, and review their roles in the induction and progression of chronic airway inflammation in both mice and human systems.
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Endo, Y. et al. (2016). Human and Mouse Memory-Type Pathogenic Th2 (Tpath2) Cells in Airway Inflammation. In: Miyasaka, M., Takatsu, K. (eds) Chronic Inflammation. Springer, Tokyo. https://doi.org/10.1007/978-4-431-56068-5_31
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DOI: https://doi.org/10.1007/978-4-431-56068-5_31
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