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Related Experiment Video

Updated: May 14, 2026

Flow Cytometry-Based Isolation and Therapeutic Evaluation of Tumor-Infiltrating Lymphocytes in a Mouse Model of Pancreatic Cancer
07:55

Flow Cytometry-Based Isolation and Therapeutic Evaluation of Tumor-Infiltrating Lymphocytes in a Mouse Model of Pancreatic Cancer

Published on: January 17, 2025

Cardiolipin Induces CXCL9/CXCL10 Expression in Tumor-Infiltrating Lymphocytes.

Joana R Lérias1, Eric de Sousa1, Carolina M Gorgulho1

  • 1Immunotherapy/ImmunoSurgery Laboratory, Cell Center (Champalimaud Foundation), Avenida Brasília, 1400-038 Lisbon, Portugal.

Cells
|May 13, 2026
PubMed
Summary

Cardiolipin (CL) activates tumor-infiltrating lymphocytes (TIL) via the NLRP3 inflammasome pathway, enhancing their ability to recognize cancer mutations. This suggests CL may be a danger signal that aids TIL expansion in gastrointestinal cancer.

Keywords:
T-cell receptor (TCR)cardiolipincytokinesgastrointestinal cancermitochondriamutant mitochondriapancreatic cancerpeptide recognitiontumor-associated antigen (TAA)tumor-infiltrating lymphocytes (TIL)

Related Experiment Videos

Last Updated: May 14, 2026

Flow Cytometry-Based Isolation and Therapeutic Evaluation of Tumor-Infiltrating Lymphocytes in a Mouse Model of Pancreatic Cancer
07:55

Flow Cytometry-Based Isolation and Therapeutic Evaluation of Tumor-Infiltrating Lymphocytes in a Mouse Model of Pancreatic Cancer

Published on: January 17, 2025

Area of Science:

  • Immunology
  • Cancer Biology
  • Mitochondrial Biology

Background:

  • Cardiolipin (CL) is a crucial phospholipid in the inner mitochondrial membrane and bacterial membranes.
  • CL release during cell death and inflammation suggests a role in danger signaling.
  • Its potential to activate tumor-infiltrating lymphocytes (TIL) in epithelial cancers was investigated.

Purpose of the Study:

  • To determine if cardiolipin (CL) can activate and expand tumor-infiltrating lymphocytes (TIL) from gastrointestinal cancer patients.
  • To investigate the role of the NLRP3 inflammasome in CL-mediated TIL activation.
  • To assess the impact of CL on TIL recognition of tumor-specific mutations.

Main Methods:

  • TIL were isolated and expanded in vitro with CL.
  • NLRP3 inflammasome activity was assessed using MCC950 inhibitor and NLRP3 siRNA.
  • T-cell potency was measured by CXCL9/10 expression; immune repertoire was analyzed by deep TCR sequencing.
  • Recognition of autologous tumor cells and mutations (KRAS, UQCRFS1 D145V) was evaluated using MHC restriction assays.

Main Results:

  • CL expansion increased TIL expression of CXCL9/10, indicating enhanced tissue invasion potential.
  • CL-expanded TIL showed broader recognition of KRAS mutations, blocked by NLRP3 inhibition.
  • TIL exhibited an enriched TCR repertoire and recognized autologous tumor cells, including a mutant mitochondrial protein (UQCRFS1 D145V).

Conclusions:

  • Cardiolipin activates the NLRP3 inflammasome pathway in TIL from GI cancer patients.
  • CL enhances TIL expression of CXCL9/10, leading to improved recognition of mutant cancer epitopes, including mitochondrial targets.
  • CL may act as a danger signal, facilitating TIL expansion through CL-activated pathways.