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10.4049/jimmunol.0903075

http://scihub22266oqcxt.onion/10.4049/jimmunol.0903075
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C2924920!2924920!20656925
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suck abstract from ncbi


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pmid20656925      J+Immunol 2010 ; 185 (5): 2980-8
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  • The Migration of T cells in Response to Influenza Virus is Altered in Neonatal Mice #MMPMID20656925
  • Lines JL; Hoskins S; Hollifield M; Cauley LS; Garvy BA
  • J Immunol 2010[Sep]; 185 (5): 2980-8 PMID20656925show ga
  • 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 days 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 days post-infection, whereas neonatal T cell infiltration, activation and expression of TNF? was delayed until 2 weeks post-infection. While 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, while the chemokines CXCL1, CXCL9 and CCL2 remained at baseline levels and CCL11 was highly elevated. Intranasal administration of CCL2, IFN?, 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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