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Updated: Mar 21, 2026

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Effector T Cells Abrogate Stroma-Mediated Chemoresistance in Ovarian Cancer

Weimin Wang1, Ilona Kryczek2, Lubomír Dostál3

  • 1Department of Obstetrics and Gynecology, University of Michigan School of Medicine, Ann Arbor, MI 48109, USA; Department of Surgery, University of Michigan School of Medicine, Ann Arbor, MI 48109, USA.

Cell
|May 3, 2016
PubMed

Insights

Fibroblasts cause chemotherapy resistance in ovarian cancer by reducing platinum in cells. Effector T cells overcome this resistance by altering fibroblast metabolism, offering new treatment strategies.

Area of Science:

  • Oncology
  • Immunology
  • Cell Biology

Background:

  • Tumor microenvironment comprises effector T cells and fibroblasts.
  • Mechanisms of cellular interactions influencing chemoresistance remain unclear.

Purpose of the Study:

  • Investigate how fibroblasts and T cells impact chemoresistance in ovarian cancer.
  • Elucidate the role of cellular interactions in platinum-based chemotherapy resistance.

Main Methods:

  • Assessed platinum accumulation in ovarian cancer cells.
  • Analyzed the role of glutathione and cysteine released by fibroblasts.
  • Studied the effect of CD8(+) T cells on fibroblast metabolism.
  • Investigated the signaling pathways (JAK/STAT1) and molecules (IFNγ) involved.

Main Results:

  • Fibroblasts reduce platinum nuclear accumulation in ovarian cancer cells, causing chemoresistance.
  • Fibroblast-derived glutathione and cysteine mediate this resistance.
  • CD8(+) T cells reverse chemoresistance by modulating fibroblast glutathione and cystine metabolism via IFNγ signaling.
  • Stromal fibroblasts correlate with poor patient survival, while CD8(+) T cells correlate with improved survival.

Conclusions:

  • Effector T cells counteract stromal fibroblast-mediated chemoresistance in ovarian cancer.
  • Targeting the interplay between chemotherapy and immunotherapy presents a promising therapeutic avenue.

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