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Related Concept Videos

Immune Response Against Viral Pathogens01:29

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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.
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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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T cells are integral to our adaptive immune system, recognizing and effectively responding to foreign antigens. T cell activation and clonal selection are pivotal in orchestrating this immune response. This article elucidates these mechanisms, detailing the roles of cluster of differentiation (CD) markers, major histocompatibility complex (MHC) molecules, costimulatory signals, and the process of clonal selection.
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Antigens Involved in Adaptive Immunity01:26

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An antigen is any substance the immune system identifies as foreign and potentially harmful to the body, prompting an immune response. Antigens have two functional properties: immunogenicity and reactivity. Immunogenicity is the ability of an antigen to stimulate a specific immune response. At the same time, reactivity describes the antigen's ability to react with the cells and antibodies produced in response to it.
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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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Multiple cell-type interactions drive invariant NKT cell hepatitis.

Jiaxin Tan1,2, Longshan Ji1,2, Qian Li1,2

  • 1Laboratory of Cellular Immunity, Shanghai Key Laboratory of Traditional Chinese Medicine, Shuguang Hospital Affiliated to Shanghai University of Traditional Chinese Medicine, Key Laboratory of Liver and Kidney Diseases (Shanghai University of Traditional Chinese Medicine), Ministry of Education, Shanghai, China.

Hepatology Communications
|March 25, 2025
PubMed
Summary

Myeloid cells, including neutrophils and macrophages, drive α-Galcer-induced NKT hepatitis. Targeting myeloid cell infiltration offers a potential therapeutic strategy for NKT cell-mediated liver injury.

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Use of Single Chain MHC Technology to Investigate Co-agonism in Human CD8+ T Cell Activation
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Area of Science:

  • Immunology
  • Hepatology
  • Cell Biology

Background:

  • α-Galactosylceramide (α-Galcer) activates invariant natural killer T (NKT) cells, showing promise in antitumor therapy.
  • α-Galcer treatment can cause acute hepatitis due to NKT cell accumulation in the liver.
  • Mechanisms of NKT-mediated hepatitis are not fully understood, prompting investigation into myeloid cell involvement.

Purpose of the Study:

  • To investigate the role of myeloid cells in α-Galcer-induced NKT hepatitis.
  • To elucidate the molecular mechanisms by which myeloid cells contribute to NKT cell-mediated liver injury.

Main Methods:

  • Utilized α-Galcer-induced NKT hepatitis mouse models.
  • Generated and studied microRNA-223 (miR-223) and neutrophil cytosolic factor 1 (Ncf1)-deficient mice.

Main Results:

  • α-Galcer induced neutrophil and macrophage accumulation in the liver, with elevated inflammatory mediators.
  • Inhibiting myeloid cell migration (via CXCR2, CCR2, CCR5) reduced liver injury by decreasing reactive oxygen species and inflammation.
  • Neutrophil depletion lessened liver injury; miR-223 deficiency exacerbated, while Ncf1 deficiency ameliorated, inflammation and oxidative damage.

Conclusions:

  • Neutrophil and macrophage infiltration are crucial for NKT cell activation-induced hepatitis.
  • This study highlights myeloid cell infiltration's role in NKT cell-mediated liver injury.
  • Findings suggest novel therapeutic strategies for NKT cell hepatitis by targeting myeloid cell infiltration.