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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.
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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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The intestinal epithelial lining rapidly renews every 4 to 5 days. The renewal is facilitated by intestinal stem cells (ISCs) located at the base of the crypt– a gland located at the bottom of each villus. ISCs divide asymmetrically to form new stem cells and progenitor daughter cells. The daughter cells are called transit-amplifying (TA) cells which move upwards along the crypt and either differentiate into absorptive cells– the enterocytes or secretory cells– including the...
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Visualization of IL-22-expressing Lymphocytes Using Reporter Mice
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Interleukin-22 Promotes Cell Proliferation to Combat Virus Infection in Human Intestinal Epithelial Cells.

Cuncai Guo1, Ashwini Kumar Sharma1,2, José Guzmán1

  • 1Department of Infectious Diseases, Virology, Heidelberg University Hospital, Heidelberg, Germany.

Journal of Interferon & Cytokine Research : the Official Journal of the International Society for Interferon and Cytokine Research
|July 30, 2024
PubMed
Summary

Interferon lambdas (IFN-λs) and Interleukin-22 (IL-22) independently protect human intestinal cells. IFN-λs induce antiviral genes, while IL-22 promotes cell proliferation for epithelial repair.

Keywords:
interferoninterleukin-22intestinal epithelial cellslambdaorganoids

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Area of Science:

  • Immunology
  • Virology
  • Gastroenterology

Background:

  • Interferon lambdas (IFN-λs) are vital for controlling viral infections at mucosal surfaces.
  • Interleukin-22 (IL-22) may enhance IFN-λ's antiviral activity in the gut through ISG induction or cell proliferation.
  • The synergistic effects of IL-22 and IFN-λ in human intestinal epithelial cells (IECs) remain unclear.

Purpose of the Study:

  • To investigate the potential synergistic effects of IL-22 and IFN-λ in human IEC models.
  • To elucidate the distinct roles of IL-22 and IFN-λ in antiviral defense and epithelial homeostasis.

Main Methods:

  • Co-treatment of human IECs with IL-22 and IFN-λ.
  • Analysis of STAT1 phosphorylation and interferon-stimulated genes (ISGs) expression.
  • Transcriptomics analysis to compare signaling pathways.
  • Assessment of IL-22's effect on human intestinal organoid proliferation and stem cell marker expression.

Main Results:

  • Co-treatment with IL-22 and IFN-λ increased STAT1 phosphorylation but did not enhance ISG production or antiviral protection.
  • Transcriptomics revealed independent signaling pathways: IFN-λ induces ISGs, while IL-22 promotes cell proliferation.
  • IL-22 significantly increased human intestinal organoid size via cell proliferation and OLFM4 expression.

Conclusions:

  • In human IECs, IL-22 and IFN-λ act independently rather than synergistically to combat viral infections.
  • IFN-λ controls viral replication by inducing ISGs, whereas IL-22 facilitates epithelial repair and clearance of infected cells through proliferation.
  • Both cytokines play crucial, distinct roles in protecting the human intestinal epithelium.