Literature DB >> 21887154

Central role of dendritic cells in shaping the adaptive immune response during respiratory syncytial virus infection.

Daniel S McDermott1, Kayla A Weiss, Cory J Knudson, Steven M Varga.   

Abstract

Respiratory syncytial virus (RSV) is the leading cause of lower respiratory tract disease in young children. Premature infants, immunocompromised individuals and the elderly exhibit the highest risk for the development of severe RSV-induced disease. Murine studies demonstrate that CD8 T cells mediate RSV clearance from the lungs. Murine studies also indicate that the host immune response contributes to RSV-induced morbidity as T-cell depletion prevents the development of disease despite sustained viral replication. Dendritic cells (DCs) play a central role in the induction of the RSV-specific adaptive immune response. Following RSV infection, lung-resident DCs acquire viral antigens, migrate to the lung-draining lymph nodes and initiate the T-cell response. This article focuses on data generated from both in vitro DC infection studies and RSV mouse models that together have advanced our understanding of how RSV infection modulates DC function and the subsequent impact on the adaptive immune response.

Entities:  

Year:  2011        PMID: 21887154      PMCID: PMC3163480          DOI: 10.2217/fvl.11.62

Source DB:  PubMed          Journal:  Future Virol        ISSN: 1746-0794            Impact factor:   1.831


  70 in total

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6.  Differential response of human naive and memory/effector T cells to dendritic cells infected by respiratory syncytial virus.

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3.  Upregulation of H3K27 Demethylase KDM6 During Respiratory Syncytial Virus Infection Enhances Proinflammatory Responses and Immunopathology.

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Review 6.  Immunological, Viral, Environmental, and Individual Factors Modulating Lung Immune Response to Respiratory Syncytial Virus.

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Review 7.  Modulation of Respiratory TLR3-Anti-Viral Response by Probiotic Microorganisms: Lessons Learned from Lactobacillus rhamnosus CRL1505.

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Review 8.  Functional Impairment of Mononuclear Phagocyte System by the Human Respiratory Syncytial Virus.

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