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Protein Signature Differentiating Neutrophils and Myeloid-Derived Suppressor Cells Determined Using a Human Isogenic

Yuting Zhang1,2, Jin Hu3, Xiashiyao Zhang4

  • 1Department of Biological Sciences, Boler-Parseghian Center for Rare and Neglected Diseases, Harper Cancer Research Institute, University of Notre Dame, Notre Dame, IN 46556, USA.

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|May 24, 2024
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Summary

Myeloid-derived suppressor cells (MDSCs) hinder anti-tumor immunity. This study identified protein signatures to distinguish MDSCs from normal cells, offering potential biomarkers and therapeutic targets for immunotherapy enhancement.

Keywords:
immunotherapymass spectrometrymyeloid-derived suppressor cellprotein signatureproteomics

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Area of Science:

  • Immunology and Cancer Biology
  • Proteomics and Mass Spectrometry

Background:

  • Myeloid-derived suppressor cells (MDSCs) are crucial in suppressing anti-tumor T lymphocyte activity in solid tumors, making them a key target for immunotherapy.
  • Distinguishing MDSCs from their counterparts, like polymorphonuclear neutrophils (PMNs), is challenging due to shared markers, necessitating advanced proteomic characterization.
  • Existing markers for MDSCs are limited, highlighting the need for comprehensive proteomic studies to identify reliable signature proteins.

Purpose of the Study:

  • To identify novel protein signatures that differentiate MDSCs from normal myeloid cells (PMNs and monocytes).
  • To discover potential protein biomarkers for specific MDSC identification.
  • To uncover potential therapeutic targets for impairing MDSC function in cancer immunotherapy.

Main Methods:

  • Induced differentiation of human promyelocytic cell line HL60 into isogenic PMNs (iPMNs) and MDSCs (iMDSCs).
  • Global and membrane proteomics profiling of iPMNs, iMDSCs, and HL60 using quantitative mass spectrometry.
  • Integration of cell line proteomics data with published datasets from primary human monocytes and cancer-associated fibroblast-induced MDSCs.

Main Results:

  • A 41-protein signature ('cluster 6') was identified as upregulated in iMDSCs compared to HL60 and iPMNs.
  • An integrated analysis revealed a 38-protein signature upregulated in MDSCs compared to normal monocytes and PMNs.
  • These identified protein signatures offer a basis for distinguishing MDSCs and developing targeted therapies.

Conclusions:

  • Proteomic analysis successfully identified distinct protein signatures for MDSCs.
  • These signatures can serve as a foundation for developing biomarkers to phenotypically distinguish MDSCs from healthy myeloid cells.
  • The findings provide potential therapeutic targets to selectively impair MDSCs, thereby enhancing cancer immunotherapy efficacy without harming normal myeloid cells.