tetano
Editor, Senior Moderator
Eur J Immunol. 2013 Nov 12. doi: 10.1002/eji.201343587. [Epub ahead of print]
CD11c+ cells primed with unrelated antigens facilitate an accelerated immune response to influenza virus in mice.
Richert LE, Rynda-Apple A, Harmsen AL, Han S, Wiley JA, Douglas T, Larson K, Morton RV, Harmsen AG.
Source
Department of Immunology and Infectious Diseases, Montana State University, Bozeman, Montana, USA.
Abstract
Recent evidence suggests that an individual's unique history and sequence of exposures to pathogens and antigens may dictate downstream immune responses to disparate antigens. We show that the intranasal delivery of non-replicative virus-like particles (VLPs), which bear structural but no antigenic similarities to respiratory pathogens, acts to prime the lungs of both C56BL/6 and BALB/c mice, facilitating heightened and accelerated primary immune responses to high-dose influenza challenge, thus providing a non-pathogenic model of innate imprinting. These responses correspond closely to those observed following natural infection with the opportunistic fungus, Pneumocystis murina, and are characterized by accelerated antigen processing by dendritic cells (DCs) and alveolar macrophages (AMs), an enhanced influx of cells to the local tracheobronchial lymph node (TBLN), and early upregulation of T-cell co-stimulatory/adhesion molecules. CD11c+ cells which have been directly exposed to VLPs or Pneumocystis are necessary in facilitating enhanced clearance of influenza virus, and the repopulation of the lung by Ly-6C+ precursors relies on CCR2 expression. Thus, immune imprinting 72 hours after VLP-, or 2 weeks after Pneumocystis-priming is CCR2-mediated and results from the enhanced antigen processing, maturation, and trafficking abilities of DCs and AMs, which cause accelerated influenza-specific primary immune responses and result in superior viral clearance. This article is protected by copyright. All rights reserved.
This article is protected by copyright. All rights reserved.
KEYWORDS:
CCR2, Dendritic cell, Influenza, Innate imprinting, Pneumocystis murina
PMID:
24222381
[PubMed - as supplied by publisher]
http://www.ncbi.nlm.nih.gov/pubmed/24222381
CD11c+ cells primed with unrelated antigens facilitate an accelerated immune response to influenza virus in mice.
Richert LE, Rynda-Apple A, Harmsen AL, Han S, Wiley JA, Douglas T, Larson K, Morton RV, Harmsen AG.
Source
Department of Immunology and Infectious Diseases, Montana State University, Bozeman, Montana, USA.
Abstract
Recent evidence suggests that an individual's unique history and sequence of exposures to pathogens and antigens may dictate downstream immune responses to disparate antigens. We show that the intranasal delivery of non-replicative virus-like particles (VLPs), which bear structural but no antigenic similarities to respiratory pathogens, acts to prime the lungs of both C56BL/6 and BALB/c mice, facilitating heightened and accelerated primary immune responses to high-dose influenza challenge, thus providing a non-pathogenic model of innate imprinting. These responses correspond closely to those observed following natural infection with the opportunistic fungus, Pneumocystis murina, and are characterized by accelerated antigen processing by dendritic cells (DCs) and alveolar macrophages (AMs), an enhanced influx of cells to the local tracheobronchial lymph node (TBLN), and early upregulation of T-cell co-stimulatory/adhesion molecules. CD11c+ cells which have been directly exposed to VLPs or Pneumocystis are necessary in facilitating enhanced clearance of influenza virus, and the repopulation of the lung by Ly-6C+ precursors relies on CCR2 expression. Thus, immune imprinting 72 hours after VLP-, or 2 weeks after Pneumocystis-priming is CCR2-mediated and results from the enhanced antigen processing, maturation, and trafficking abilities of DCs and AMs, which cause accelerated influenza-specific primary immune responses and result in superior viral clearance. This article is protected by copyright. All rights reserved.
This article is protected by copyright. All rights reserved.
KEYWORDS:
CCR2, Dendritic cell, Influenza, Innate imprinting, Pneumocystis murina
PMID:
24222381
[PubMed - as supplied by publisher]
http://www.ncbi.nlm.nih.gov/pubmed/24222381