| First Author | Guo XJ | Year | 2018 |
| Journal | Immunity | Volume | 49 |
| Issue | 3 | Pages | 531-544.e6 |
| PubMed ID | 30170813 | Mgi Jnum | J:277557 |
| Mgi Id | MGI:6284415 | Doi | 10.1016/j.immuni.2018.07.011 |
| Citation | Guo XJ, et al. (2018) Lung gammadelta T Cells Mediate Protective Responses during Neonatal Influenza Infection that Are Associated with Type 2 Immunity. Immunity 49(3):531-544.e6 |
| abstractText | Compared to adults, infants suffer higher rates of hospitalization, severe clinical complications, and mortality due to influenza infection. We found that gammadelta T cells protected neonatal mice against mortality during influenza infection. gammadelta T cell deficiency did not alter viral clearance or interferon-gamma production. Instead, neonatal influenza infection induced the accumulation of interleukin-17A (IL-17A)-producing gammadelta T cells, which was associated with IL-33 production by lung epithelial cells. Neonates lacking IL-17A-expressing gammadelta T cells or Il33 had higher mortality upon influenza infection. gammadelta T cells and IL-33 promoted lung infiltration of group 2 innate lymphoid cells and regulatory T cells, resulting in increased amphiregulin secretion and tissue repair. In influenza-infected children, IL-17A, IL-33, and amphiregulin expression were correlated, and increased IL-17A levels in nasal aspirates were associated with better clinical outcomes. Our results indicate that gammadelta T cells are required in influenza-infected neonates to initiate protective immunity and mediate lung homeostasis. |
