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Related Experiment Video

Updated: Jul 29, 2025

Author Spotlight: A Model to Study the Systemic and Local Dynamics of CD8+ T Cells During LN Metastasis
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Tumor-activated lymph node fibroblasts suppress T cell function in diffuse large B cell lymphoma.

Benedetta Apollonio1, Filomena Spada2, Nedyalko Petrov2

  • 1School of Cancer and Pharmaceutical Sciences, Faculty of Life Sciences & Medicine, King's College London, London, United Kingdom.

The Journal of Clinical Investigation
|May 23, 2023
PubMed
Summary

Fibroblastic reticular cells (FRCs) in diffuse large B cell lymphoma (DLBCL) create an immunosuppressive tumor microenvironment, hindering T cell function. Targeting FRCs with FAP-targeted therapies can enhance anti-lymphoma immunity.

Keywords:
Cancer immunotherapyImmunologyLymphomasOncology

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Area of Science:

  • Immunology
  • Oncology
  • Cell Biology

Background:

  • Transcriptomic analysis of diffuse large B cell lymphoma (DLBCL) implicates lymph node (LN) fibroblast and tumor-infiltrating lymphocyte (TIL) signatures in the tumor microenvironment (TME).
  • The specific immunomodulatory functions of fibroblasts within the lymphoma context remain largely undefined.

Purpose of the Study:

  • To investigate the role of fibroblastic reticular cells (FRCs) in the DLBCL tumor microenvironment.
  • To determine how DLBCL influences FRC function and its impact on T cell-mediated immunity.
  • To explore therapeutic strategies targeting FRCs to enhance anti-lymphoma responses.

Main Methods:

  • Analysis of human and mouse DLBCL-LNs to characterize FRC networks and fibroblast-activated protein (FAP) expression.
  • RNA-sequencing (RNA-Seq) to assess FRC pathway reprogramming upon DLBCL exposure.
  • Functional assays to evaluate the effect of DLBCL-activated FRCs (DLBCL-FRCs) on T cell migration and cytotoxicity.
  • Imaging mass cytometry to analyze CD8+ TIL-FRC interactions and spatial organization in patient LNs.
  • In vitro co-treatment experiments using FAP-targeted drugs and bispecific antibodies (glofitamab) on organotypic cultures.

Main Results:

  • Identified aberrantly remodeled FRC networks with elevated FAP expression in DLBCL-LNs.
  • DLBCL exposure reprogrammed FRCs towards inflammatory chemokine production and enhanced antigen presentation.
  • DLBCL-FRCs impaired T cell migration and suppressed CD8+ TIL cytotoxicity in an antigen-specific manner.
  • Distinct CD8+ TIL-FRC spatial organizations in patient LNs correlated with survival outcomes.
  • Combined FAP-targeted therapy and glofitamab boosted anti-lymphoma TIL cytotoxicity in organotypic cultures.

Conclusions:

  • FRCs play a significant immunosuppressive role in DLBCL, contributing to immune evasion and disease pathogenesis.
  • Targeting FRCs, particularly FAP-expressing ones, represents a promising strategy to enhance T cell-based immunotherapies for DLBCL patients.
  • Understanding TIL-FRC interactions is crucial for optimizing treatment strategies and improving patient outcomes.