The migration of T cells in response to influenza virus is altered in neonatal mice

J. Louise Lines, Samantha Hoskins, Melissa Hollifield, Linda S. Cauley, Beth A. Garvy

Research output: Contribution to journalArticlepeer-review

43 Scopus citations


Influenza virus is a significant cause of mortality and morbidity in children; however, little is known about the T cell response in infant lungs. Neonatal mice are highly vulnerable to influenza and only control very low doses of virus. We compared the T cell response to influenza virus infection between mice infected as adults or at 2 d old and observed defective migration into the lungs of the neonatal mice. In the adult mice, the numbers of T cells in the lung interstitia peaked at 10 d postinfection, whereas neonatal T cell infiltration, activation, and expression of TNF-α was delayed until 2 wk postinfection. Although T cell numbers ultimately reached adult levels in the interstitia, they were not detected in the alveoli of neonatal lungs. Instead, the alveoli contained eosinophils and neutrophils. This altered infiltrate was consistent with reduced or delayed expression of type 1 cytokines in the neonatal lung and differential chemokine expression. In influenza-infected neonates, CXCL2, CCL5, and CCL3 were expressed at adult levels, whereas the chemokines CXCL1, CXCL9, and CCL2 remained at baseline levels, and CCL11 was highly elevated. Intranasal administration of CCL2, IFN-γ, or CXCL9 was unable to draw the neonatal T cells into the airways. Together, these data suggest that the T cell response to influenza virus is qualitatively different in neonatal mice and may contribute to an increased morbidity.

Original languageEnglish
Pages (from-to)2980-2988
Number of pages9
JournalJournal of Immunology
Issue number5
StatePublished - Sep 1 2010

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology


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