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Vaccinations

Vaccinations

Hepatitis

Hepatitis

Hepatitis is an inflammatory condition of the liver most commonly caused by hepatotropic viruses (A–E), though non-infectious causes such as alcohol and drugs also exist.Hepatitis AHepatitis A virus (HAV) is a non-enveloped RNA virus of the Picornaviridae family. It is primarily transmitted via the fecal-oral route, typically through ingestion of contaminated food or water. After ingestion, HAV enters the bloodstream through the oropharynx or intestinal epithelium and reaches the liver.

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Updated: Apr 14, 2026

Stem Cell-Derived Viral Ag-Specific T Lymphocytes Suppress HBV Replication in Mice

Stem Cell-Derived Viral Ag-Specific T Lymphocytes Suppress HBV Replication in Mice

Published on: September 25, 2019

CD8 positive T-cells decrease neurogenesis and induce anxiety-like behaviour following hepatitis B vaccination.

Tuo Zhou¹, Yuxuan Gao², Zhiling Wang³

¹Children's Health Section, Guangzhou Women and Children's Medical Center, Guangzhou Medical University, Guangzhou 510623, China.

Brain Communications

|October 10, 2024

Summary

This summary is machine-generated.

Hepatitis B vaccination impacts brain function, increasing anxiety and reducing neurogenesis via CD8+ T cells. Glial cells recruit these T cells, affecting mood and memory.

Keywords:

CXCL16 CXCR6 TNF-α hepatitis B vaccine neurogenesis

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Induction and Diverse Assessment Indicators of Experimental Autoimmune Encephalomyelitis

Induction and Diverse Assessment Indicators of Experimental Autoimmune Encephalomyelitis

Published on: September 9, 2022

Area of Science:

Neuroimmunology
Neuroscience
Immunology

Background:

Peripheral immune system influences brain function, including neuronal development and cognition.
Previous research linked hepatitis B vaccination to reduced hippocampal neurogenesis and spatial memory.
Understanding vaccine-induced immunity's effects on neuropsychiatric disorders is crucial.

Purpose of the Study:

Investigate mechanisms of T cell subsets modulating hippocampal neurogenesis and anxiety-like behaviors post-hepatitis B vaccination.
Identify key T cell subsets and molecular pathways involved.

Main Methods:

Utilized hepatitis B vaccine-induced T cells in immunodeficient mice.
Administered T cells and analyzed behavioral changes (anxiety-like behaviors).
Assessed hippocampal cell proliferation and performed transcriptome profiling of CD8+ T cells.

Main Results:

Hepatitis B vaccine-T cell recipients showed increased anxiety and decreased hippocampal cell proliferation.
CD8+ T cells, not CD4+ T cells, were the primary mediators of these effects.
CXCR6+ CD8+ T cells infiltrated the brain via CXCL16 from glial cells, impairing neurogenesis and inducing anxiety through TNF-α.

Conclusions:

Glial CXCL16 mediates the brain recruitment of CXCR6+ CD8+ T cells following hepatitis B vaccination.
This mechanism links vaccination to altered neurogenesis and anxiety-like behaviors.
Targeting this pathway may offer therapeutic strategies for mood and cognitive regulation.