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Related Concept Videos

Immune Response Against Viral Pathogens01:29

Immune Response Against Viral Pathogens

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The immune system's response to viral infections is a complex and coordinated process involving natural killer (NK) cells, T cell-mediated responses, and antibody-mediated responses.
NK Cells
NK cells are a crucial part of our innate immune system, acting as the first line of defense against viral infections. These cells can recognize and kill infected cells without prior exposure to the virus, effectively slowing down the spread of infection. Additionally, NK cells produce proinflammatory...
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When T cells with CD4 markers are activated, they give rise to two types of effector cells: helper T cells and regulatory T cells. Meanwhile, T cells with CD8 markers differentiate into effector cytotoxic T cells. The differentiation of CD4 T cells into helper T cell subsets, such as Th1, Th2, and Th17 cells, is dependent on the antigen type, antigen-presenting cell, and regulatory cytokines.
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Cytotoxic T cells are a vital component of the immune system. They have the remarkable ability to identify and target antigens on infected or abnormal cells. These antigens often originate from intracellular pathogens such as viruses or abnormal proteins cancer cells produce.
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Immunotherapy is a treatment that boosts or manipulates the immune system to fight diseases, including cancer. For instance, by stimulating an immune response through vaccinations against viruses that cause cancers, like hepatitis B virus and human papillomavirus, these diseases can be prevented. Nonetheless, some cancer cells can avoid the immune system due to their rapid mutation and division. The immune response to many cancers involves three phases: elimination, equilibrium, and escape.
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Multivesicular bodies (MVBs) are mature endosomes that sort ubiquitinated proteins and then fuse with lysosomes to degrade the sorted proteins. Epidermal growth factor (EGF) and its receptor (EGFR) form a complex that can be internalized through endocytosis, sorted into an MVB, and later degraded.
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STING Restricts EV-A71 Infection by Regulating T Cell Development and Enhancing Immune Cell Effector Function.

Huiqiang Wang1,2, Ya Wang1,2, Shuo Wu1,2,3

  • 1CAMS Key Laboratory of Antiviral Drug Research, Beijing Key Laboratory of Technology and Application for Anti-Infective New Drugs Research and Development, NHC Key Laboratory of Biotechnology of Antibiotics, Institute of Medicinal Biotechnology, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100050, China.

International Journal of Molecular Sciences
|December 11, 2025
PubMed
Summary
This summary is machine-generated.

Activating STING inhibits Enterovirus A71 (EV-A71) replication in vivo, improving survival. STING knockout worsens EV-A71 infection, highlighting STING

Keywords:
EV-A71STINGdiABZIimmune regulationinflammation

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Area of Science:

  • Immunology
  • Virology
  • Molecular Biology

Background:

  • Enterovirus A71 (EV-A71) infection can activate STING signaling pathways in vitro.
  • The in vivo role of STING and its immune regulatory mechanisms in EV-A71 infection are not fully understood.

Purpose of the Study:

  • To investigate the role and mechanism of STING in regulating EV-A71 infection in vivo.
  • To explore STING's impact on immune responses during EV-A71 infection.

Main Methods:

  • Utilized STING-specific agonist diABZI to activate STING.
  • Employed STING-knockout mice to assess STING's function in EV-A71 infection.
  • Analyzed viral replication, clinical symptoms, survival rates, immune cell populations, and cytokine profiles.

Main Results:

  • STING activation inhibited EV-A71 replication, reduced symptoms, and increased survival in mice.
  • STING knockout exacerbated viral replication, lethality, and disease severity.
  • STING activation promoted interferon signaling, upregulated interferon-stimulated genes (ISGs), modulated cytokine profiles, and expanded immune cell populations (T cells, NK cells, myeloid cells).
  • STING knockout impaired T cell development and reduced CD8+ T cell and NK cell effector functions.

Conclusions:

  • STING activation effectively suppresses EV-A71 replication and alleviates infection symptoms by modulating immune and inflammatory responses.
  • Findings provide a framework for understanding STING's role in antiviral immunity.
  • Suggests potential for STING-targeted therapies against viral infections.