scholarly journals Fucosyltransferase Induction during Influenza Virus Infection Is Required for the Generation of Functional Memory CD4+ T Cells

2018 ◽  
Vol 200 (8) ◽  
pp. 2690-2702 ◽  
Author(s):  
Roberto Tinoco ◽  
Florent Carrette ◽  
Monique L. Henriquez ◽  
Yu Fujita ◽  
Linda M. Bradley
Keyword(s):  
T Cells ◽  
Influenza Virus ◽  
Virus Infection ◽  
Cd4 T Cells ◽  
Influenza Virus Infection ◽  
Memory Cd4 T Cells

Antibodies and CD4+ T-cells mediate cross-protection against H5N1 influenza virus infection in mice after vaccination with a low pathogenic H5N2 strain

Vaccine ◽  
2008 ◽  
Vol 26 (52) ◽  
pp. 6965-6974 ◽  
Author(s):  
Karoline Droebner ◽  
Emanuel Haasbach ◽  
Cordula Fuchs ◽  
Andreas O. Weinzierl ◽  
Stefan Stevanovic ◽  
...  
Keyword(s):  
T Cells ◽  
Influenza Virus ◽  
Virus Infection ◽  
Cd4 T Cells ◽  
Influenza Virus Infection ◽  
Cross Protection ◽  
H5n1 Influenza Virus ◽  
H5n1 Influenza

scholarly journals Activated CD4+ T cells and CD14hiCD16+ monocytes correlate with antibody response following influenza virus infection in humans

2021 ◽  
pp. 100237
Author(s):  
Sook-San Wong ◽  
Christine M. Oshansky ◽  
Xi-Zhi J. Guo ◽  
Jacqui Ralston ◽  
Timothy Wood ◽  
...  
Keyword(s):  
T Cells ◽  
Influenza Virus ◽  
Virus Infection ◽  
Antibody Response ◽  
Cd4 T Cells ◽  
Influenza Virus Infection

scholarly journals Memory CD4 T Cells Direct Protective Responses to Influenza Virus in the Lungs through Helper-Independent Mechanisms

2010 ◽  
Vol 84 (18) ◽  
pp. 9217-9226 ◽  
Author(s):  
John R. Teijaro ◽  
David Verhoeven ◽  
Carly A. Page ◽  
Damian Turner ◽  
Donna L. Farber
Keyword(s):  
T Cells ◽  
Influenza Virus ◽  
T Cell ◽  
Cd4 T Cells ◽  
Natural Infection ◽  
Influenza Virus Infection ◽  
Cd4 T Cell ◽  
Virus Challenge ◽  
Specific Memory ◽  
Memory Cd4 T Cells

ABSTRACT Memory CD4 T cells specific for influenza virus are generated from natural infection and vaccination, persist long-term, and recognize determinants in seasonal and pandemic influenza virus strains. However, the protective potential of these long-lived influenza virus-specific memory CD4 T cells is not clear, including whether CD4 T-cell helper or effector functions are important in secondary antiviral responses. Here we demonstrate that memory CD4 T cells specific for H1N1 influenza virus directed protective responses to influenza virus challenge through intrinsic effector mechanisms, resulting in enhanced viral clearance, recovery from sublethal infection, and full protection from lethal challenge. Mice with influenza virus hemagglutinin (HA)-specific memory CD4 T cells or polyclonal influenza virus-specific memory CD4 T cells exhibited protection from influenza virus challenge that occurred in the presence of CD8-depleting antibodies in B-cell-deficient mice and when CD4 T cells were transferred into lymphocyte-deficient RAG2−/− mice. Moreover, the presence of memory CD4 T cells mobilized enhanced T-cell recruitment and immune responses in the lung. Neutralization of gamma interferon (IFN-γ) production in vivo abrogated memory CD4 T-cell-mediated protection from influenza virus challenge by HA-specific memory T cells and heterosubtypic protection by polyclonal memory CD4 T cells. Our results indicate that memory CD4 T cells can direct enhanced protection from influenza virus infection through mobilization of immune effectors in the lung, independent of their helper functions. These findings have important implications for the generation of universal influenza vaccines by promoting long-lived protective CD4 T-cell responses.

scholarly journals Cytokine-Dependent Induction of CD4+ T cells with Cytotoxic Potential during Influenza Virus Infection

2013 ◽  
Vol 87 (21) ◽  
pp. 11884-11893 ◽  
Author(s):  
L. Hua ◽  
S. Yao ◽  
D. Pham ◽  
L. Jiang ◽  
J. Wright ◽  
...  
Keyword(s):  
T Cells ◽  
Influenza Virus ◽  
Virus Infection ◽  
Cd4 T Cells ◽  
Influenza Virus Infection ◽  
Cytotoxic Potential

scholarly journals Antigen-Specific Memory Regulatory CD4+Foxp3+ T Cells Control Memory Responses to Influenza Virus Infection

2013 ◽  
Vol 190 (7) ◽  
pp. 3438-3446 ◽  
Author(s):  
Erik L. Brincks ◽  
Alan D. Roberts ◽  
Tres Cookenham ◽  
Stewart Sell ◽  
Jacob E. Kohlmeier ◽  
...  
Keyword(s):  
T Cells ◽  
Influenza Virus ◽  
Virus Infection ◽  
Influenza Virus Infection ◽  
Specific Memory

scholarly journals Cross-Reactive, Cell-Mediated Immunity and Protection of Chickens from Lethal H5N1 Influenza Virus Infection in Hong Kong Poultry Markets

2001 ◽  
Vol 75 (6) ◽  
pp. 2516-2525 ◽  
Author(s):  
Sang Heui Seo ◽  
Robert G. Webster
Keyword(s):  
T Cells ◽  
Influenza Virus ◽  
Hong Kong ◽  
Virus Infection ◽  
Cellular Immunity ◽  
Influenza Virus Infection ◽  
Influenza Viruses ◽  
H5n1 Influenza Virus ◽  
H9n2 Influenza Virus ◽  
H5n1 Influenza

ABSTRACT In 1997, avian H5N1 influenza virus transmitted from chickens to humans resulted in 18 confirmed infections. Despite harboring lethal H5N1 influenza viruses, most chickens in the Hong Kong poultry markets showed no disease signs. At this time, H9N2 influenza viruses were cocirculating in the markets. We investigated the role of H9N2 influenza viruses in protecting chickens from lethal H5N1 influenza virus infections. Sera from chickens infected with an H9N2 influenza virus did not cross-react with an H5N1 influenza virus in neutralization or hemagglutination inhibition assays. Most chickens primed with an H9N2 influenza virus 3 to 70 days earlier survived the lethal challenge of an H5N1 influenza virus, but infected birds shed H5N1 influenza virus in their feces. Adoptive transfer of T lymphocytes or CD8+ T cells from inbred chickens (B2/B2) infected with an H9N2 influenza virus to naive inbred chickens (B2/B2) protected them from lethal H5N1 influenza virus. In vitro cytotoxicity assays showed that T lymphocytes or CD8+ T cells from chickens infected with an H9N2 influenza virus recognized target cells infected with either an H5N1 or H9N2 influenza virus in a dose-dependent manner. Our findings indicate that cross-reactive cellular immunity induced by H9N2 influenza viruses protected chickens from lethal infection with H5N1 influenza viruses in the Hong Kong markets in 1997 but permitted virus shedding in the feces. Our findings are the first to suggest that cross-reactive cellular immunity can change the outcome of avian influenza virus infection in birds in live markets and create a situation for the perpetuation of H5N1 influenza viruses.

scholarly journals Ex Vivo Phenotype and Frequency of Influenza Virus-Specific CD4 Memory T Cells

2004 ◽  
Vol 78 (13) ◽  
pp. 7284-7287 ◽  
Author(s):  
Michaela Lucas ◽  
Cheryl L. Day ◽  
Jessica R. Wyer ◽  
Sharon L. Cunliffe ◽  
Andrew Loughry ◽  
...  
Keyword(s):  
T Cells ◽  
Influenza Virus ◽  
Cd4 T Cells ◽  
Memory T Cells ◽  
Ex Vivo ◽  
Class Ii ◽  
Low Frequencies ◽  
Tetramer Staining ◽  
Specific Memory ◽  
Memory Cd4 T Cells

ABSTRACT Recent advances in class II tetramer staining technology have allowed reliable direct ex vivo visualization of antigen-specific CD4 T cells. In order to define the frequency and phenotype of a prototype response to a nonpersistent pathogen, we have used such techniques to analyze influenza virus-specific memory CD4 T cells directly from blood. These responses are stably detectable ex vivo at low frequencies (range, 0.00012 to 0.0061% of CD4 T cells) and display a distinct “central memory” CD62L+ phenotype.

scholarly journals Dendritic Cells Targeting Lactobacillus plantarum Strain NC8 with a Surface-Displayed Single-Chain Variable Fragment of CD11c Induce an Antigen-Specific Protective Cellular Immune Response

2019 ◽  
Vol 88 (2) ◽  
Author(s):  
Jing Liu ◽  
Guilian Yang ◽  
Haibin Huang ◽  
Chunwei Shi ◽  
Xing Gao ◽  
...  
Keyword(s):  
T Cells ◽  
Dendritic Cells ◽  
Influenza Virus ◽  
Virus Infection ◽  
Lactobacillus Plantarum ◽  
Influenza Virus Infection ◽  
Cell Culture Supernatant ◽  
Single Chain ◽  
Ifn Γ

ABSTRACT Influenza A virus (H1N1) is an acute, highly contagious respiratory virus. The use of lactic acid bacteria (LAB) to deliver mucosal vaccines against influenza virus infection is a research hot spot. In this study, two recombinant Lactobacillus plantarum strains expressing hemagglutinin (HA) alone or coexpressing aCD11c-HA to target HA protein to dendritic cells (DCs) by fusion to an anti-CD11c single-chain antibody (aCD11c) were constructed. The activation of bone marrow dendritic cells (BMDCs) by recombinant strains and the interaction of activated BMDCs and sorted CD4+ or CD8+ T cells were evaluated through flow cytometry in vitro, and cellular supernatants were assessed by using an enzyme-linked immunosorbent assay kit. The results demonstrated that, compared to the HA strain, the aCD11c-HA strain significantly increased the activation of BMDCs and increased the production of CD4+ gamma interferon-positive (IFN-γ+) T cells, CD8+ IFN-γ+ T cells, and IFN-γ in the cell culture supernatant in vitro. Consistent with these results, the aCD11c-HA strain clearly increased the activation and maturation of DCs, the HA-specific responses of CD4+ IFN-γ+ T cells, CD8+ IFN-γ+ T cells, and CD8+ CD107a+ T cells, and the proliferation of T cells in the spleen, finally increasing the levels of specific antibodies and neutralizing antibodies in mice. In addition, the protection of immunized mice was observed after viral infection, as evidenced by improved weight loss, survival, and lung pathology. The adoptive transfer of CD8+ T cells from the aCD11c-HA mice to NOD/Lt-SCID mice resulted in a certain level of protection after influenza virus infection, highlighting the efficacy of the aCD11c targeting strategy.

scholarly journals Deficiency of the NOD-Like Receptor NLRC5 Results in Decreased CD8+ T Cell Function and Impaired Viral Clearance

2017 ◽  
Vol 91 (17) ◽  
Author(s):  
Christopher R. Lupfer ◽  
Kate L. Stokes ◽  
Teneema Kuriakose ◽  
Thirumala-Devi Kanneganti
Keyword(s):  
T Cells ◽  
Influenza Virus ◽  
T Cell ◽  
Virus Infection ◽  
Adaptive Immune Response ◽  
Influenza Virus Infection ◽  
Viral Clearance ◽  
Mhc I ◽  
Adaptive Immune ◽  
Pathogen Recognition Receptors

ABSTRACT Pathogen recognition receptors are vital components of the immune system. Engagement of these receptors is important not only for instigation of innate immune responses to invading pathogens but also for initiating the adaptive immune response. Members of the NOD-like receptor (NLR) family of pathogen recognition receptors have important roles in orchestrating this response. The NLR family member NLRC5 regulates major histocompatibility complex class I (MHC-I) expression during various types of infections, but its role in immunity to influenza A virus (IAV) is not well studied. Here we show that Nlrc5 −/− mice exhibit an altered CD8+ T cell response during IAV infection compared to that of wild-type (WT) mice. Nlrc5 −/− mice have decreased MHC-I expression on hematopoietic cells and fewer CD8+ T cells prior to infection. NLRC5 deficiency does not affect the generation of antigen-specific CD8+ T cells following IAV infection; however, a change in epitope dominance is observed in Nlrc5 −/− mice. Moreover, IAV-specific CD8+ T cells from Nlrc5 −/− mice have impaired effector functions. This change in the adaptive immune response is associated with impaired viral clearance in Nlrc5 −/− mice. Collectively, our results demonstrate an important role for NLRC5 in regulation of antiviral immune responses and viral clearance during IAV infection. IMPORTANCE The NOD-like receptor family member NLRC5 is known to regulate expression of MHC-I as well as other genes required for antigen processing. In addition, NLRC5 also regulates various immune signaling pathways. In this study, we investigated the role of NLRC5 during influenza virus infection and found a major role for NLRC5 in restricting virus replication and promoting viral clearance. The observed increases in viral titers in NLRC5-deficient mice correlated with impaired effector CD8+ T cell responses. Although NLRC5-deficient mice were defective at clearing the virus, they did not show an increase in morbidity or mortality following influenza virus infection because of other compensatory immune mechanisms. Therefore, our study highlights how NLRC5 regulates multiple immune effector mechanisms to promote the host defense during influenza virus infection.

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