Spatial transcriptomics and immunophenotyping uncover chronic inflammation-induced immune adaptations favoring dysplasia development in patients at risk of colitis-associated cancer - Takeaways - MDSpire

Spatial transcriptomics and immunophenotyping uncover chronic inflammation-induced immune adaptations favoring dysplasia development in patients at risk of colitis-associated cancer

  • By

  • Sofía Frigerio

  • Hina N Khan

  • Mojtaba Amini

  • Bregje Mol

  • Andra Neefjes-Borst

  • Manon E Wildenberg

  • Cyriel Y Ponsioen

  • Geert R D’Haens

  • Yvonne Vercoulen

  • Joep Grootjans

  • October 13, 2025

  • 0 min

Share

  • 1

    Colitis-associated cancer (CAC) is a severe complication of inflammatory bowel disease (IBD) linked to chronic inflammation and dysplasia.

  • 2

    Chronic inflammation induces immune cell reprogramming that undermines immunosurveillance, increasing the risk of CAC in IBD patients.

  • 3

    Increased IL-10 expression by IgA+ plasma cells and CD163+ macrophages represents endogenous anti-inflammatory mechanisms in CAC.

  • 4

    Decreased CD8+ intraepithelial T cells (IELs) and granzyme B levels correlate with CAC susceptibility in IBD patients.

  • 5

    Chronic inflammation may limit inflammation but also reduces immunosurveillance, favoring the development of CAC.

Original Source(s)

Spatial transcriptomics and immunophenotyping uncover chronic inflammation-induced immune adaptations favoring dysplasia development in patients at risk of colitis-associated cancer

  • by Sofía Frigerio, Hina N Khan, Mojtaba Amini, Bregje Mol, Andra Neefjes-Borst, Manon E Wildenberg, Cyriel Y Ponsioen, Geert R D’Haens, Yvonne Vercoulen, Joep Grootjans

  • October 13, 2025

Related Content

Evaluation of 5-Aminosalicylic Acid Utilization in Crohn’s Disease Management: Insights from a Nationwide Survey of Inflammatory Bowel Disease Specialists

Refining Vancomycin Use in Early CDI

A modified dosing approach could reshape recurrence prevention strategies.

Renal Conditions Associated with Inflammatory Bowel Disease: Exploring Clinical Links, Shared Mechanisms, and Management Approaches