| First Author | You D | Year | 2013 |
| Journal | J Leukoc Biol | Volume | 93 |
| Issue | 6 | Pages | 933-42 |
| PubMed ID | 23543769 | Mgi Jnum | J:201209 |
| Mgi Id | MGI:5512794 | Doi | 10.1189/jlb.1012498 |
| Citation | You D, et al. (2013) IL-4Ralpha on CD4+ T cells plays a pathogenic role in respiratory syncytial virus reinfection in mice infected initially as neonates. J Leukoc Biol 93(6):933-42 |
| abstractText | RSV is the major cause of severe bronchiolitis in infants, and severe bronchiolitis as a result of RSV is associated with subsequent asthma development. A biased Th2 immune response is thought to be responsible for neonatal RSV pathogenesis; however, molecular mechanisms remain elusive. Our data demonstrate, for the first time, that IL-4Ralpha is up-regulated in vitro on human CD4(+) T cells from cord blood following RSV stimulation and in vivo on mouse pulmonary CD4(+) T cells upon reinfection of mice, initially infected as neonates. Th cell-specific deletion of Il4ra attenuated Th2 responses and abolished the immunopathophysiology upon reinfection, including airway hyper-reactivity, eosinophilia, and mucus hyperproduction in mice infected initially as neonates. These findings support a pathogenic role for IL-4Ralpha on Th cells following RSV reinfection of mice initially infected as neonates; more importantly, our data from human cells suggest that the same mechanism occurs in humans. |
