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Circulating and Tumor-Infiltrating NK Cells From Clear Cell Renal Cell Carcinoma Patients Exhibit a Predominantly

Andrea Ziblat1, Ximena Lucía Raffo Iraolagoitia1, Sol Yanel Nuñez1

  • 1Laboratorio de Fisiopatología de la Inmunidad Innata, Instituto de Biología y Medicina Experimental (IBYME-CONICET), Buenos Aires, Argentina.

Frontiers in Immunology
|June 21, 2021
PubMed

Insights

Natural killer (NK) cells in kidney cancer (ccRCC) show dysfunction. Researchers identified specific cell markers on peripheral blood NK cells that can distinguish ccRCC patients from healthy donors, suggesting new biomarkers and immunotherapy targets.

Area of Science:

  • Immunology
  • Oncology
  • Renal Cell Carcinoma Research

Background:

  • Natural killer (NK) cells are crucial immune cells that infiltrate clear cell renal cell carcinomas (ccRCC).
  • Despite infiltration, NK cells often become dysfunctional within the tumor microenvironment, hindering anti-tumor immunity.
  • Understanding NK cell phenotypic changes in ccRCC is vital for identifying new biomarkers and therapeutic targets.

Purpose of the Study:

  • To perform a detailed phenotypic analysis of peripheral blood NK cells (PBNK) and tumor-infiltrating NK cells (TINK) in ccRCC patients.
  • To identify potential biomarkers and immunotherapy targets by analyzing NK cell surface marker expression.
  • To correlate NK cell marker expression with ccRCC patient status and NK cell infiltration.

Main Methods:

  • Phenotypic analysis of PBNK and TINK from ccRCC patients and healthy donors (HD) using flow cytometry.
  • Analysis of The Cancer Genome Atlas (TCGA) data to assess gene expression in ccRCC tumors.
  • Statistical analysis, including z-score calculations, to identify distinguishing markers.

Main Results:

  • PBNK from ccRCC patients showed increased expression of CD25, CD69, CD62L, DNAM-1, CD48, CD45, MHC-I, and PD-1, with reduced NKG2D and increased CD85j+
  • TINK exhibited higher activation markers and tissue residency features but decreased expression of activating receptors (DNAM-1, NKp30, NKp46, NKp80, CD16), indicating an inhibitory phenotype.
  • TCGA analysis revealed significant overexpression of CD48, CD45, CD85j, and PD-1 in ccRCC, associated with NK cell infiltration signatures. These markers, particularly on PBNK, differentiated ccRCC patients from HD.

Conclusions:

  • Specific phenotypic markers on NK cells, including CD48, CD45, CD85j, and PD-1, are altered in ccRCC patients.
  • These markers, especially when evaluated on PBNK, show potential as novel biomarkers for distinguishing ccRCC patients from healthy individuals.
  • The identified markers represent promising targets for developing novel immunotherapies to enhance anti-tumor responses in ccRCC.
Keywords:
CD45CD48CD85jNK cellsPD-1renal cell carcinoma

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