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Age-Dependent Cell Trafficking Defects in Draining Lymph Nodes Impair Adaptive Immunity and Control of West Nile Virus Infection
Journal article   Open access   Peer reviewed

Age-Dependent Cell Trafficking Defects in Draining Lymph Nodes Impair Adaptive Immunity and Control of West Nile Virus Infection

Justin M. Richner, Grzegorz B. Gmyrek, Jennifer Govero, Yizheng Tu, Gerritje J. W. van der Windt, Talibah U. Metcalf, Elias K. Haddad, Johannes Textor, Mark J. Miller and Michael S. Diamond
PLoS pathogens, v 11(7), pp e1005027-e1005027
01 Jul 2015
PMID: 26204259
url
https://journals.plos.org/plospathogens/article/file?id=10.1371/journal.ppat.1005027&type=printableView
Published, Version of Record (VoR) Open
url
https://doi.org/10.1371/journal.ppat.1005027View
Published, Version of Record (VoR) Open

Abstract

Life Sciences & Biomedicine Microbiology Parasitology Science & Technology Virology
Impaired immune responses in the elderly lead to reduced vaccine efficacy and increased susceptibility to viral infections. Although several groups have documented age-dependent defects in adaptive immune priming, the deficits that occur prior to antigen encounter remain largely unexplored. Herein, we identify novel mechanisms for compromised adaptive immunity that occurs with aging in the context of infection with West Nile virus (WNV), an encephalitic flavivirus that preferentially causes disease in the elderly. An impaired IgM and IgG response and enhanced vulnerability to WNV infection during aging was linked to delayed germinal center formation in the draining lymph node (DLN). Adoptive transfer studies and two-photon intravital microscopy revealed a decreased trafficking capacity of donor naive CD4(+) T cells from old mice, which manifested as impaired T cell diapedesis at high endothelial venules and reduced cell motility within DLN prior to antigen encounter. Furthermore, leukocyte accumulation in the DLN within the first few days of WNV infection or antigen-adjuvant administration was diminished more generally in old mice and associated with a second aging-related defect in local cytokine and chemokine production. Thus, age-dependent cell-intrinsic and environmental defects in the DLN result in delayed immune cell recruitment and antigen recognition. These deficits compromise priming of early adaptive immune responses and likely contribute to the susceptibility of old animals to acute WNV infection.

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Collaboration types
Domestic collaboration
International collaboration
Web of Science research areas
Microbiology
Parasitology
Virology
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