scholarly journals Recombinant BCG-Prime and DNA-Boost Immunization Confers Mice with Enhanced Protection against Mycobacterium kansasii

Vaccines ◽  
2021 ◽  
Vol 9 (11) ◽  
pp. 1260
Author(s):  
Shihoko Komine-Aizawa ◽  
Satoru Mizuno ◽  
Kazuhiro Matsuo ◽  
Takahiro Namiki ◽  
Satoshi Hayakawa ◽  
...  
Keyword(s):  
T Cells ◽  
Cd8 T Cells ◽  
Multidrug Resistant ◽  
Mycobacterium Kansasii ◽  
Booster Immunization ◽  
Boost Vaccination ◽  
Antigen 85B ◽  
Boost Immunization ◽  
Potential Alternative ◽  
Mouse Lungs

The incidence of infections with nontuberculous mycobacteria (NTM) has been increasing worldwide. The emergence of multidrug-resistant NTM is a serious clinical concern, and a vaccine for NTM has not yet been developed. We previously developed a new recombinant Bacillus Calmette–Guérin (rBCG) vaccine encoding the antigen 85B (Ag85B) protein of Mycobacterium kansasii—termed rBCG-Mkan85B—which was used together with a booster immunization with plasmid DNA expressing the same M. kansasii Ag85B gene (DNA-Mkan85B). We reported that rBCG-Mkan85B/DNA-Mkan85B prime–boost immunization elicited various NTM strain-specific CD4+ and CD8+ T cells and induced Mycobacterium tuberculosis-specific immunity. In this study, to investigate the protective effect against M. kansasii infection, we challenged mice vaccinated with a rBCG-Mkan85B or rBCG-Mkan85B/DNA-Mkan85B prime–boost strategy with virulent M. kansasii. Although BCG and rBCG-Mkan85B immunization each suppressed the growth of M. kansasii in the mouse lungs, the rBCG-Mkan85B/DNA-Mkan85B prime–boost vaccination reduced the bacterial burden more significantly. Moreover, the rBCG-Mkan85B/DNA-Mkan85B prime–boost vaccination induced antigen-specific CD4+ and CD8+ T cells. Our data suggest that rBCG-Mkan85B/DNA-Mkan85B prime–boost vaccination effectively enhances antigen-specific T cells. Our novel rBCG could be a potential alternative to clinical BCG for preventing various NTM infections.

scholarly journals IL-17A Expression in HIV-Specific CD8 T Cells Is Regulated by IL-4/IL-13 Following HIV-1 Prime-Boost Immunization

2015 ◽  
Vol 35 (3) ◽  
pp. 176-185 ◽  
Author(s):  
Jayashree Ravichandran ◽  
Ronald J. Jackson ◽  
Shubhanshi Trivedi ◽  
Charani Ranasinghe
Keyword(s):  
T Cells ◽  
Cd8 T Cells ◽  
Boost Immunization ◽  
Hiv 1

scholarly journals Mycobacterium tuberculosis Multidrug Resistant Strain M Induces an Altered Activation of Cytotoxic CD8+ T Cells

PLoS ONE ◽  
2014 ◽  
Vol 9 (5) ◽  
pp. e97837 ◽  
Author(s):  
Laura Geffner ◽  
Juan Ignacio Basile ◽  
Noemí Yokobori ◽  
Denise Kviatcovsky ◽  
Carmen Sabio y García ◽  
...  
Keyword(s):  
T Cells ◽  
Mycobacterium Tuberculosis ◽  
Cd8 T Cells ◽  
Resistant Strain ◽  
Multidrug Resistant ◽  
Multidrug Resistant Strain

scholarly journals Broad anti-SARS-CoV-2 antibody immunity induced by heterologous ChAdOx1/mRNA-1273 prime-boost vaccination

2021 ◽  
Author(s):  
Chengzi I Kaku ◽  
Elizabeth Champney ◽  
Johan Normark ◽  
Carl E Johnson ◽  
Clas Ahlm ◽  
...  
Keyword(s):  
Monoclonal Antibodies ◽  
B Cell ◽  
Molecular Basis ◽  
Booster Vaccination ◽  
Neutralizing Antibody ◽  
Binding Affinities ◽  
Booster Immunization ◽  
Boost Vaccination ◽  
Immunization Strategies ◽  
Boost Immunization

Heterologous prime-boost immunization strategies have the potential to augment COVID-19 vaccine efficacy and address ongoing vaccine supply challenges. Here, we longitudinally profiled SARS-CoV-2 spike (S)-specific serological and memory B cell (MBC) responses in individuals receiving either homologous (ChAdOx1:ChAdOx1) or heterologous (ChAdOx1:mRNA-1273) prime-boost vaccination. Heterologous mRNA booster immunization induced significantly higher serum neutralizing antibody and MBC responses compared to homologous ChAdOx1 boosting. Specificity mapping of circulating S-specific B cells revealed that mRNA-1273 booster immunization dramatically immunofocused ChAdOx1-primed responses onto epitopes expressed on prefusion-stabilized S. Monoclonal antibodies isolated from mRNA-1273-boosted participants displayed higher binding affinities and increased breadth of reactivity against variants of concern (VOCs) relative to those isolated from ChAdOx1-boosted participants. Overall, the results provide fundamental insights into the B cell response induced by ChAdOx1 and a molecular basis for the enhanced immunogenicity observed following heterologous mRNA booster vaccination.

scholarly journals Prime-Boost Immunization Eliminates Metastatic Colorectal Cancer by Producing High-Avidity Effector CD8+T Cells

2017 ◽  
Vol 198 (9) ◽  
pp. 3507-3514 ◽  
Author(s):  
Bo Xiang ◽  
Trevor R. Baybutt ◽  
Lisa Berman-Booty ◽  
Michael S. Magee ◽  
Scott A. Waldman ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
T Cells ◽  
Metastatic Colorectal Cancer ◽  
Cd8 T Cells ◽  
High Avidity ◽  
Boost Immunization

scholarly journals Airway delivery of both a BCG prime and adenoviral boost drives CD4 and CD8 T cells into the lung tissue parenchyma

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Daryan A. Kaveh ◽  
M. Carmen Garcia-Pelayo ◽  
Naomi C. Bull ◽  
Pedro J. Sanchez-Cordon ◽  
John Spiropoulos ◽  
...  
Keyword(s):  
T Cells ◽  
Lung Tissue ◽  
Cd8 T Cells ◽  
Murine Model ◽  
Vaccine Development ◽  
Lung Parenchyma ◽  
Boost Vaccination ◽  
Parenteral Delivery ◽  
Promising Strategy ◽  
Intravascular Staining

Abstract Heterologous BCG prime-boost regimens represent a promising strategy for an urgently required improved tuberculosis vaccine. Identifying the mechanisms which underpin the enhanced protection induced by such strategies is one key aim which would significantly accelerate rational vaccine development. Experimentally, airway vaccination induces greater efficacy than parenteral delivery; in both conventional vaccination and heterologous boosting of parenteral BCG immunisation. However, the effect of delivering both the component prime and boost immunisations via the airway is not well known. Here we investigate delivery of both the BCG prime and adenovirus boost vaccination via the airway in a murine model, and demonstrate this approach may be able to improve the protective outcome over parenteral prime/airway boost. Intravascular staining of T cells in the lung revealed that the airway prime regimen induced more antigen-specific multifunctional CD4 and CD8 T cells to the lung parenchyma prior to challenge and indicated the route of both prime and boost to be critical to the location of induced resident T cells in the lung. Further, in the absence of a defined phenotype of vaccine-induced protection to tuberculosis; the magnitude and phenotype of vaccine-specific T cells in the parenchyma of the lung may provide insights into potential correlates of immunity.

scholarly journals Mucosal HIV-1 Pox Virus Prime-Boost Immunization Induces High-Avidity CD8+ T Cells with Regime-Dependent Cytokine/Granzyme B Profiles

2007 ◽  
Vol 178 (4) ◽  
pp. 2370-2379 ◽  
Author(s):  
Charani Ranasinghe ◽  
Stephen J. Turner ◽  
Craig McArthur ◽  
Duncan B. Sutherland ◽  
Jee-Hye Kim ◽  
...  
Keyword(s):  
T Cells ◽  
Cd8 T Cells ◽  
Granzyme B ◽  
High Avidity ◽  
Boost Immunization ◽  
Hiv 1

LFA-1 is required for retention of effector CD8 T cells in mouse lungs

Blood ◽  
2003 ◽  
Vol 101 (12) ◽  
pp. 4916-4922 ◽  
Author(s):  
Jayant Thatte ◽  
Vrushali Dabak ◽  
Mark B. Williams ◽  
Thomas J. Braciale ◽  
Klaus Ley
Keyword(s):  
T Cells ◽  
Cell Adhesion ◽  
Adhesion Molecule ◽  
Cd8 T Cells ◽  
Cell Clone ◽  
Intercellular Adhesion Molecule ◽  
Lymphocyte Function ◽  
T Cell Clone ◽  
Mouse Lungs

AbstractThe adhesion molecules involved in the migration and retention of activated effector CD8 T cells in the lung microcirculation and their recruitment into lung tissue are largely unknown. Here, we have analyzed the role of lymphocyte function–associated antigen-1 (LFA-1) and very late antigen-4 (VLA-4) on adhesion of influenza hemagglutinin (HA)–specific CD8 T-cell clone D4 under shear conditions in an in vitro binding assay and in an in vivo homing assay to the lungs of naive or transgenic Balb/c mice expressing HA (HA-Tg) by a lung-specific promoter. Blocking LFA-1 or intercellular adhesion molecule 1 (ICAM-1) significantly inhibited adhesion of D4 cells to lung vascular endothelium and parenchyma of lung sections. However, blocking VLA-4 or vascular cell adhesion molecule 1 (VCAM-1) had no effect on cell adhesion. Blocking LFA-1 in vivo significantly delayed lethal injury following adoptive transfer of D4 cells into HA-Tg mice as assessed by weight loss and histology. Residence time of adoptively transferred Indium 111 (111In)–labeled D4 cells in lungs of normal and HA-Tg mice as analyzed by dual modality imaging revealed a significantly shorter transit time of 4 hours for the D4 cells upon in vivo blockade of LFA-1. These results demonstrate a crucial role for LFA-1 in retention of activated CD8 T cells in normal mouse lungs and in the progression of lethal injury in HA-Tg mice.

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