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Molecular and Cellular Mechanisms of Vaccine-Induced Immune Responses

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Immunology".

Deadline for manuscript submissions: 31 August 2026 | Viewed by 1026

Special Issue Editor


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Guest Editor
Division of Vaccine Development Coordination, Center for Vaccine Research National Institute of Infectious Diseses, Korea National Institute of Health, Korea Disease Control and Prevention Agency, Cheongju-si, Republic of Korea
Interests: viral genomics and evolution; molecular mechanisms of host adaptation; virus–host protein interactions; genetic determinants of viral pathogenicity; immune evasion and viral mutation
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Special Issue Information

Dear Colleagues,

Vaccination remains one of the most effective public health interventions for the prevention and control of infectious diseases. Recent advances in vaccine platforms—including mRNA vaccines, viral vectors, recombinant protein vaccines, and novel adjuvant systems—have greatly expanded our ability to induce protective immune responses against diverse pathogens. However, the molecular and cellular mechanisms by which vaccines initiate, shape, and sustain immune responses remain incompletely understood and often vary depending on vaccine composition, delivery platform, and host factors.

At the molecular level, vaccine-derived antigens interact with innate immune sensors and antigen-presenting cells, activating signaling pathways that regulate antigen processing, presentation, and downstream adaptive immune responses. At the cellular level, the quality and durability of vaccine-induced protection depend on the coordinated activation of innate immune cells, B cells, CD4⁺ and CD8⁺ T cells, and the formation of immunological memory. Differences in these mechanisms can critically influence vaccine efficacy, breadth of protection, and safety profiles, particularly in the context of emerging pathogens, antigenic variation, and repeated booster immunization.

As global efforts increasingly focus on pandemic preparedness and rapid vaccine development, there is a growing need to integrate molecular, cellular, and systems-level immunology to better understand vaccine-induced immunity. Such mechanistic insights are essential for rational vaccine design, optimization of adjuvants and vaccination strategies, identification of immune correlates of protection, and the development of next-generation vaccines.

This Special Issue aims to provide a focused platform for original research articles and comprehensive reviews that advance our understanding of the molecular and cellular mechanisms underlying vaccine-induced immune responses. We welcome studies that elucidate how different vaccine platforms and formulations engage innate and adaptive immune pathways, shape immune memory, and influence vaccine efficacy and safety.

Topics of interest include, but are not limited to, molecular signaling pathways activated by vaccine antigens and adjuvants; antigen processing and presentation mechanisms; innate immune sensing and trained immunity; B-cell and T-cell activation, differentiation, and memory formation; immune correlates of protection; systems immunology and multi-omics approaches to vaccine response profiling; and host factors influencing variability in vaccine-induced immunity. Studies addressing immune responses to vaccines against emerging or re-emerging pathogens, as well as comparative analyses across vaccine platforms, are particularly encouraged.

Dr. In Ohk Ouh
Guest Editor

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Keywords

  • vaccine platforms
  • molecular mechanisms
  • innate immune sensing
  • adaptive immune responses
  • adjuvants and signaling pathways
  • antigen processing and presentation
  • immunological memory
  • systems immunology

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Published Papers (1 paper)

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Research

13 pages, 2579 KB  
Article
Genotype-Dependent Virulence of Severe Fever with Thrombocytopenia Syndrome Virus in a Mouse Challenge Model
by Eun Bee Choi, Seungyeon Kim, Seo Young Moon, Eun Young Jang, Yookyoung Lee and In-Ohk Ouh
Int. J. Mol. Sci. 2026, 27(7), 3148; https://doi.org/10.3390/ijms27073148 - 30 Mar 2026
Viewed by 484
Abstract
Severe fever with thrombocytopenia syndrome (SFTS) is an emerging tick-borne infectious disease with high case-fatality rates in East Asia. The causative agent, SFTS virus (SFTSV; also known as Dabie bandavirus), exhibits genotype-dependent differences in pathogenicity. However, infection models that recapitulate these variations and [...] Read more.
Severe fever with thrombocytopenia syndrome (SFTS) is an emerging tick-borne infectious disease with high case-fatality rates in East Asia. The causative agent, SFTS virus (SFTSV; also known as Dabie bandavirus), exhibits genotype-dependent differences in pathogenicity. However, infection models that recapitulate these variations and can be applied for vaccine and therapeutic evaluation are still lacking. In this study, we assessed the pathogenicity of two Korean SFTSV isolates representing the F and B genotypes in a murine infection model. Wild-type C57BL/6 and IFNAR knockout (IFNAR−/−) mice were intraperitoneally infected with two different doses of SFTSV (2 and 2 × 10−1 FFU). All C57BL/6 mice survived regardless of viral genotype or dose. In IFNAR−/− mice, infection with either F- or B-type virus at the 2 FFU dose resulted in mortality beginning at 5 days post-infection, with all mice succumbing within 6 days. At the higher dose (2 × 10−1 FFU), mortality differed by genotype: B-type infection led to 20% lethality, whereas F-type infection caused 40% lethality by day 5. Infected and deceased mice exhibited body weight loss as a characteristic clinical outcome. Collectively, these findings demonstrate genotype-associated differences in SFTSV pathogenicity in mice and establish a murine challenge model that may be useful for the preclinical evaluation of candidate vaccines and antiviral agents. Full article
(This article belongs to the Special Issue Molecular and Cellular Mechanisms of Vaccine-Induced Immune Responses)
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