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

Authors: Lines, JL  Hoskins, S  Hollifield, M  Cauley, LS  Garvy, BA 
Citation: Lines JL, etal., J Immunol. 2010 Sep 1;185(5):2980-8. Epub 2010 Jul 23.
Pubmed: (View Article at PubMed) PMID:20656925
DOI: Full-text: DOI:10.4049/jimmunol.0903075

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-alpha 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-gamma, 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.


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RGD Object Information
RGD ID: 4145452
Created: 2010-11-04
Species: All species
Last Modified: 2010-11-04
Status: ACTIVE


RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.