| First Author | Reuter S | Year | 2016 |
| Journal | Cell Immunol | Volume | 308 |
| Pages | 27-34 | PubMed ID | 27372382 |
| Mgi Jnum | J:335031 | Mgi Id | MGI:6760372 |
| Doi | 10.1016/j.cellimm.2016.06.003 | Citation | Reuter S, et al. (2016) Cylindromatosis (Cyld) gene mutation in T cells promotes the development of an IL-9-dependent allergic phenotype in experimental asthma. Cell Immunol 308:27-34 |
| abstractText | Cylindromatosis (CYLD) is a ubiquitously expressed deubiquitinating enzyme which removes activating ubiquitin residues from important signaling molecules of the NF-kappaB pathway. In CYLD(ex7/8) transgenic mice, a naturally occurring short isoform (sCYLD) is overexpressed in the absence of full length CYLD, leading to excessive NF-kappaB activity. Herein, we investigated the impact of the CYLD(ex7/8) mutation selectively in T cells on the development of experimental allergic airway disease induced by sensitization and challenge with ovalbumin. Compared with their wildtype littermates, mice bearing the T cell-specific mutation (CD4(+)CYLD(ex7/8)) display stronger eosinophilia and mucus production in the lungs and higher IgE serum levels. The reason for these observations is excessive production of T cell-derived IL-9, a cytokine to whom allergy-promoting properties were ascribed. Consequently, blockade of IL-9 in CD4(+)CYLD(ex7/8) mice alleviates the development of disease symptoms. Thus, by polarization of the T cell cytokine response, sCYLD can favor the development of allergic airway disease. |
