scholarly journals Memory regulatory T cells home to the lung and control influenza A virus infection

2019 ◽  
Vol 97 (9) ◽  
pp. 774-786 ◽  
Author(s):  
Chunni Lu ◽  
Damien Zanker ◽  
Peter Lock ◽  
Xiangrui Jiang ◽  
Jieru Deng ◽  
...  
Keyword(s):  
T Cells ◽  
Virus Infection ◽  
Regulatory T Cells ◽  
Influenza A Virus ◽  
Influenza A ◽  
Influenza A Virus Infection ◽  
And Control

scholarly journals Type I Interferon Plays Opposing Roles in Cytotoxicity and Interferon-γ Production by Natural Killer and CD8+ T Cells after Influenza A Virus Infection in Mice

2014 ◽  
Vol 6 (4) ◽  
pp. 456-466 ◽  
Author(s):  
Yojiro Arimori ◽  
Risa Nakamura ◽  
Hisakata Yamada ◽  
Kensuke Shibata ◽  
Naoyoshi Maeda ◽  
...  
Keyword(s):  
T Cells ◽  
Virus Infection ◽  
Natural Killer ◽  
Influenza A Virus ◽  
Influenza A ◽  
Type I Interferon ◽  
Type I ◽  
Influenza A Virus Infection

scholarly journals Cutting Edge: Antigen Presentation to CD8 T Cells after Influenza A Virus Infection

2008 ◽  
Vol 182 (1) ◽  
pp. 29-33 ◽  
Author(s):  
Elizabeth Ingulli ◽  
Castle Funatake ◽  
Erica L. Jacovetty ◽  
Maurizio Zanetti
Keyword(s):  
T Cells ◽  
Virus Infection ◽  
Antigen Presentation ◽  
Influenza A Virus ◽  
Cd8 T Cells ◽  
Influenza A ◽  
Cutting Edge ◽  
Influenza A Virus Infection

High Levels of Virus-Specific CD4+T Cells Predict Severe Pandemic Influenza A Virus Infection

2012 ◽  
Vol 186 (12) ◽  
pp. 1292-1297 ◽  
Author(s):  
Yan Zhao ◽  
Yong-Hong Zhang ◽  
Laura Denney ◽  
Duncan Young ◽  
Tim J. Powell ◽  
...  
Keyword(s):  
T Cells ◽  
Virus Infection ◽  
Influenza A Virus ◽  
Pandemic Influenza ◽  
Cd4 T Cells ◽  
Influenza A ◽  
Influenza A Virus Infection

scholarly journals Highly Pathological Influenza A Virus Infection Is Associated with Augmented Expression of PD-1 by Functionally Compromised Virus-Specific CD8+ T Cells

2013 ◽  
Vol 88 (3) ◽  
pp. 1636-1651 ◽  
Author(s):  
J. A. Rutigliano ◽  
S. Sharma ◽  
M. Y. Morris ◽  
T. H. Oguin ◽  
J. L. McClaren ◽  
...  
Keyword(s):  
T Cells ◽  
Virus Infection ◽  
Influenza A Virus ◽  
Cd8 T Cells ◽  
Influenza A ◽  
Influenza A Virus Infection

scholarly journals A Detrimental Effect of Interleukin-10 on Protective Pulmonary Humoral Immunity during Primary Influenza A Virus Infection

2010 ◽  
Vol 84 (10) ◽  
pp. 5007-5014 ◽  
Author(s):  
Keer Sun ◽  
Luisa Torres ◽  
Dennis W. Metzger
Keyword(s):  
T Cells ◽  
Virus Infection ◽  
Influenza A Virus ◽  
Influenza A ◽  
Interleukin 10 ◽  
Viral Clearance ◽  
Wild Type ◽  
Passive Protection ◽  
Virus Specific Antibody ◽  
Influenza A Virus Infection

ABSTRACT Interleukin-10 (IL-10) is an important anti-inflammatory molecule that can cause immunosuppression and long-term pathogen persistence during chronic infection of mice with viruses such as lymphocytic choriomeningitis virus. However, its specific role in immunity to acute viral infections is not fully understood. We found that IL-10 plays a detrimental role in host responses to acute influenza A virus since IL-10−/− mice had improved viral clearance and survival after infection compared to wild-type mice. Enhanced viral clearance in IL-10−/− mice was not correlated with increased CD4+ or CD8+ T-cell recruitment into the lung but was correlated with increased pulmonary anti-influenza virus antibody titers, and this was dependent upon the presence of T cells, primarily CD4+ T cells. In addition, virus-specific antibody produced during the early stages of infection in the respiratory tract of IL-10−/− but not wild-type mice was sufficient to mediate passive protection against viral challenge of naïve mice. Complement was necessary for this antibody-mediated passive protection, but FcγR or neutrophil deficiency did not significantly influence viral clearance. Our results show that an absence of IL-10 at the time of primary infection leads to enhanced local virus-specific antibody production and, thus, increased protection against influenza A virus infection.

scholarly journals CC Chemokine Receptor 7 Expression by Effector/Memory CD4+ T Cells Depends on Antigen Specificity and Tissue Localization during Influenza A Virus Infection

2004 ◽  
Vol 78 (14) ◽  
pp. 7528-7535 ◽  
Author(s):  
Gudrun F. Debes ◽  
Kerstin Bonhagen ◽  
Thorsten Wolff ◽  
Ute Kretschmer ◽  
Stefan Krautwald ◽  
...  
Keyword(s):  
T Cells ◽  
Virus Infection ◽  
Influenza A Virus ◽  
Influenza A ◽  
Memory T Cells ◽  
Effector Memory ◽  
Effector Memory T Cells ◽  
Ifn Γ ◽  
Influenza A Virus Infection ◽  
Cc Chemokine Receptor 7

ABSTRACT The lung is an important entry site for respiratory pathogens such as influenza A virus. In order to combat such invading infectious agents, effector/memory T cells home to the lung and other peripheral tissues as well as lymphoid organs. In this process, chemokines and their receptors fulfill important roles in the guidance of T cells into such organs and specialized microenvironments within tissues. In this study, we determined if CD4+ T cells residing in different lung compartments and draining lymph nodes of influenza A virus-infected and naïve mice express receptors allowing their recirculation into secondary lymphoid tissues. We found high levels of l-selectin and CC chemokine receptor 7 (CCR7) expression in lung-derived CD4+ T cells, similar to that detected on T cells in secondary lymphoid organs. Upon influenza A virus infection, the bulk of gamma interferon-positive (IFN-γ+) and IFN-γ− CD4+ T cells recovered from lung parenchyma retained functional CCR7, whereas virus-specific IFN-γ-producing T cells were CCR7−. In contrast, a majority of virus-specific IFN-γ+ T cells in the lung draining lymph node were CCR7+. Independent of infection, CD4+ T cells obtained from the lung airways exhibited the lowest expression level of l-selectin and CCR7, indicating that T cells at this anatomical site represent the most differentiated effector cell type, lacking the ability to recirculate. Our results suggest that effector/memory T cells that enter inflammatory sites retain functional CCR7 expression, which is lost only upon response to viral antigen and after localization to the final effector site.

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