CD103+ intraepithelial T cells in high-grade serous ovarian cancer are phenotypically diverse TCRαβ+ CD8αβ+ T cells that can be targeted for cancer immunotherapy

Oncotarget. 2016 Nov 15;7(46):75130-75144. doi: 10.18632/oncotarget.12077.

Abstract

CD103+ tumor-infiltrating lymphocytes (TIL) have been linked to specific epithelial infiltration and a prolonged survival in high-grade serous epithelial ovarian cancer (HGSC). However, whether these cells are induced as part of an ongoing anti-HGSC immune response or represent non-specifically expanded resident or mucosal lymphocytes remains largely unknown. In this study, we first confirmed that CD103+ TIL from HGSC were predominantly localized in the cancer epithelium and were strongly correlated with an improved prognosis. We further demonstrate that CD103+ TIL were almost exclusively CD3+ TCRαβ+ CD8αβ+ CD4- T cells, but heterogeneously expressed T cell memory and differentiation markers. Activation of peripheral T cells in the presence of HGSC was sufficient to trigger induction of CD103 in over 90% of all CD8+ cells in a T cell receptor (TCR)- and TGFβR1-dependent manner. Finally, CD103+ TIL isolated from primary HGSC showed signs of recent activation and dominantly co-expressed key immunotherapeutic targets PD-1 and CD27. Taken together, our data indicate CD103+ TIL in HGSC are formed as the result of an adaptive anti-tumor immune response that might be reactivated by (dual) checkpoint inhibition.

Keywords: CD103; TGF-β; cancer immunotherapy; high-grade serous ovarian cancer; tumor-infiltrating lymphocytes.

MeSH terms

  • Antigens, CD / metabolism*
  • Biomarkers
  • CD8-Positive T-Lymphocytes*
  • Female
  • Humans
  • Immunotherapy
  • Immunotherapy, Adoptive
  • Integrin alpha Chains / metabolism*
  • Intraepithelial Lymphocytes / immunology*
  • Intraepithelial Lymphocytes / metabolism*
  • Lymphocytes, Tumor-Infiltrating*
  • Neoplasm Grading
  • Ovarian Neoplasms / immunology*
  • Ovarian Neoplasms / metabolism*
  • Ovarian Neoplasms / pathology
  • Ovarian Neoplasms / therapy
  • Phenotype
  • Prognosis
  • Programmed Cell Death 1 Receptor / metabolism
  • Protein Serine-Threonine Kinases / metabolism
  • Receptor, Transforming Growth Factor-beta Type I
  • Receptors, Antigen, T-Cell, alpha-beta / metabolism*
  • Receptors, Transforming Growth Factor beta / metabolism
  • Signal Transduction
  • Tumor Necrosis Factor Receptor Superfamily, Member 7 / metabolism

Substances

  • Antigens, CD
  • Biomarkers
  • Integrin alpha Chains
  • PDCD1 protein, human
  • Programmed Cell Death 1 Receptor
  • Receptors, Antigen, T-Cell, alpha-beta
  • Receptors, Transforming Growth Factor beta
  • Tumor Necrosis Factor Receptor Superfamily, Member 7
  • alpha E integrins
  • Protein Serine-Threonine Kinases
  • Receptor, Transforming Growth Factor-beta Type I