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Related Concept Videos

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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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Interferon-gamma induces epithelial reprogramming driving CXCL11-mediated T-cell migration.

Alessandro Cutilli1,2, Suze A Jansen1,3,4, Francesca Paolucci1,2

  • 1Regenerative Medicine Center, University Medical Center Utrecht, Uppsalalaan 8, 3584 CT Utrecht, The Netherlands.

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Interferon-gamma reprograms intestinal organoids to attract T-cells via CXCL11. This suggests targeting CXCL11 could prevent T-cell migration to inflamed intestines.

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Area of Science:

  • Immunology
  • Gastroenterology
  • Cell Biology

Background:

  • Interferon-gamma (IFN-γ) has complex roles in intestinal immunity, acting as both anti- and pro-inflammatory.
  • Understanding how epithelial cells respond to IFN-γ is crucial for modulating immune responses in the gut.

Purpose of the Study:

  • To investigate how IFN-γ exposure reprograms human intestinal epithelial organoids.
  • To determine if reprogrammed organoids can directly influence lymphocyte behavior.
  • To identify specific mechanisms by which IFN-γ impacts T-cell responses.

Main Methods:

  • Utilized a 3D co-culture system with human intestinal epithelial organoids.
  • Treated organoids with IFN-γ and analyzed transcriptional changes.
  • Performed proteomic analysis on organoid-conditioned medium.
  • Assessed T-cell migration and activation in response to treated organoids.

Main Results:

  • IFN-γ induced a pro-inflammatory gene expression profile in organoids, including CXCL9, CXCL10, and CXCL11.
  • Organoids secreted chemokines like CXCL11 after IFN-γ treatment.
  • IFN-γ-treated organoids enhanced T-cell migration, dependent on CXCL11.
  • T-cell activation status remained unchanged by the organoid treatment.

Conclusions:

  • IFN-γ reprograms intestinal epithelia towards a pro-inflammatory state.
  • CXCL11 secreted by epithelial cells is a key mediator of T-cell recruitment.
  • Targeting CXCL11 presents a potential strategy to control T-cell trafficking in inflammatory bowel diseases.