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Systems Biology to Identify Biomarkers of Neonatal Vaccine Immunogenicity [methylation]

ABSTRACT: Systems Biology to Identify Biomarkers of Neonatal Vaccine Immunogenicity [methylation]

PROVIDER: PRJNA1139074 | ENA |

REPOSITORIES: ENA

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Systems Biology to Identify Biomarkers of Neonatal Vaccine Immunogenicity [methylation]

Project description:Infection is the most common cause of death in early life, especially for newborns and can be reduced by immunization but insufficient knowledge of how vaccines protect the very young limits their optimal use. To gain insight into how vaccines induce protection of the most vulnerable, our project employs two novel approaches studying newborn responses to hepatitis B vaccine (HBV): (a) systems biology that uses technologies which comprehensively measure global changes in molecules such as transcriptomics (RNA) and proteomics (proteins), as well as cell composition of the blood and (b) use of human newborn blood components, collected prior to immunization, to model vaccine responses in vitro (outside the body). Characterizing vaccine-induced molecular patterns (signatures) that correspond to vaccine-mediated protection will accelerate development and optimization of vaccines against early life infections of major global health importance.

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Systems Biology to Identify Biomarkers of Neonatal Vaccine Immunogenicity - Papua New Guinea (PNG) Validation cohort [methylation]

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Systems Biology to Identify Biomarkers of Neonatal Vaccine Immunogenicity - Papua New Guinea (PNG) Validation cohort [methylation]

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Rules of Immunity Program: Systems Biology to Identify Biomarkers of Vaccine Immunogenicity Across the Human Lifespan

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Systems Biology of Influenza A (H5N1) Virus Monovalent Vaccine with and without AS03 adjuvant

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Systems biology analysis reveals distinct molecular signatures promoting immune responsiveness to the BNT162b COVID-19 vaccine [scRNA-seq]

Project description:Human immune responses to COVID-19 vaccines display a large heterogeneity of induced immunity and the underlying immune mechanisms for this remain largely unknown. Using a systems biology approach, we longitudinally profiled a unique cohort of female high and low responders to the BNT162b vaccine, who were known from previous COVID-19 vaccinations to develop maximum and minimum immune responses to the vaccine. We utilized high dimensional flow cytometry, bulk and single cell mRNA sequencing and 48-plex serum cytokine analyses. We revealed early, transient immunological and molecular signatures that distinguished high from low responders and correlated with B and T cell responses measured 14 days later. High responders featured a distinct transcriptional activity of interferon-driven genes and genes connected to enhanced antigen presentation. This was accompanied by a robust cytokine response related to Th1 differentiation. Both transcriptome and serum cytokine signatures were confirmed in two independent confirmatory cohorts. Collectively, our data contribute to a better understanding of the immunogenicity of mRNA-based COVID-19 vaccines, which might lead to the optimization of vaccine designs for individuals with poor vaccine responses.

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MAIT cell activation augments adenovirus vector vaccine immunogenicity

Project description:Mucosal-associated invariant T (MAIT) cells are innate sensors of viruses, which can augment early immune responses and contribute to protection from lethal infection. Thus, we reasoned MAIT cells may have an adjuvating role in the immunogenicity of replication-incompetent adenovirus vectors, which are novel vaccine platforms for pandemic pathogens such as Ebola virus and SARS-CoV-2. In both mice and human volunteers, immunization with ChAdOx1 (Chimpanzee Adenovirus Ox1) robustly activated MAIT cells. Activation required transduction of plasmacytoid dendritic cells and monocytes to produce IFN- and IL-18, respectively. IFN--induced monocyte-derived TNF was identified as a novel intermediate in this activation pathway, and activation required combinatorial signaling of all three cytokines both in vitro and in vivo. Strikingly, vaccine-induced activation of MAIT cells positively correlated with vaccine-induced T cell responses in human volunteers. Supporting a causal relationship, MAIT cell-deficient mice displayed impaired CD8+ T cell responses to multiple vaccine-encoded antigens. These findings define a novel role for MAIT cells in the immunogenicity of adenovirus vector vaccines, with potential implications for vaccine design.

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Systems biology analysis reveals distinct molecular signatures promoting immune responsiveness to the BNT162b COVID-19 vaccine [bulk RNA-seq]

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MAIT cell activation augments adenovirus vector vaccine immunogenicity

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