Regulatory T cells are critical for clearing influenza a virus in neonatal mice

Samantha Oliphant, J. Louise Lines, Melissa L. Hollifield, Beth A. Garvy

Research output: Contribution to journalArticlepeer-review

20 Scopus citations


We previously reported that neonatal mice infected with influenza A virus (IAV) develop interstitial pneumonia characterized by reduced lung cytokine and chemokine responses. The failure of T cells to infiltrate the airways of neonates correlated with delayed clearance of sublethal IAV infections compared to adults. We hypothesized that negative regulators in the neonatal lungs such as cytokines or T regulatory (Treg) cells are responsible for these differences. Neonates either deficient in interleukin-10 (IL-10) or with T cells unresponsive to transforming growth factor-β signaling due to absence of SMAD family member 4 (Smad4) had similar IAV clearance kinetics to wild-type pups and no difference in T-cell responses. In contrast, functional depletion of Treg cells with anti-CD25 monoclonal antibody resulted in increased proportions of activated CD4+ T cells in the lungs, but failure to clear IAV. Similarly, scurfy pups (mutation in forkhead box P3 [Foxp3] rendering them deficient in Treg cells) had increased proportions of activated T cells in the lungs compared to littermate controls. Scurfy pups also had increased proportions of IL-13-producing CD4+ T cells. Interestingly, like anti-CD25-treated pups, scurfy pups had significantly elevated viral loads compared to controls. Based on these data, we conclude that Tregs are critical for clearance of IAV in neonatal mice.

Original languageEnglish
Pages (from-to)580-589
Number of pages10
JournalViral Immunology
Issue number10
StatePublished - Dec 2015

Bibliographical note

Publisher Copyright:
© Mary Ann Liebert, Inc. 2015.

ASJC Scopus subject areas

  • Immunology
  • Molecular Medicine
  • Virology


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