| First Author | Endo Y | Year | 2015 |
| Journal | Immunity | Volume | 42 |
| Issue | 2 | Pages | 294-308 |
| PubMed ID | 25692703 | Mgi Jnum | J:259016 |
| Mgi Id | MGI:6141966 | Doi | 10.1016/j.immuni.2015.01.016 |
| Citation | Endo Y, et al. (2015) The interleukin-33-p38 kinase axis confers memory T helper 2 cell pathogenicity in the airway. Immunity 42(2):294-308 |
| abstractText | Memory CD4(+) T helper (Th) cells provide long-term protection against pathogens and are essential for the development of vaccines; however, some antigen-specific memory Th cells also drive immune-related pathology, including asthma. The mechanisms regulating the pathogenicity of memory Th cells remain poorly understood. We found that interleukin-33 (IL-33)-ST2 signals selectively licensed memory Th2 cells to induce allergic airway inflammation via production of IL-5 and that the p38 MAP kinase pathway was a central downstream target of IL-33-ST2 in memory Th2 cells. In addition, we found that IL-33 induced upregulation of IL-5 by memory CD4(+) T cells isolated from nasal polyps of patients with eosinophilic chronic rhinosinusitis. Thus, IL-33-ST2-p38 signaling appears to directly instruct pathogenic memory Th2 cells to produce IL-5 and induce eosinophilic inflammation. |
