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Brech, D. ; Herbstritt, A. ; Diederich, S. ; Straub, T.* ; Kokolakis, E. ; Irmler, M. ; Beckers, J. ; Büttner, F.A.* ; Schaeffeler, E.* ; Winter, S.* ; Nelson, P.J.* ; Nößner, E.

Dendritic cells or macrophages? The microenvironment of human clear cell renal cell carcinoma imprints a mosaic myeloid subtype associated with patient survival.

Cells 11:3289 (2022)

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	Open Access Gold

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Since their initial description by Elie Metchnikoff, phagocytes have sparked interest in a variety of biologic disciplines. These important cells perform central functions in tissue repair and immune activation as well as tolerance. Myeloid cells can be immunoinhibitory, particularly in the tumor microenvironment, where their presence is generally associated with poor patient prognosis. These cells are highly adaptable and plastic, and can be modulated to perform desired functions such as antitumor activity, if key programming molecules can be identified. Human clear cell renal cell carcinoma (ccRCC) is considered immunogenic; yet checkpoint blockades that target T cell dysfunction have shown limited clinical efficacy, suggesting additional layers of immunoinhibition. We previously described “enriched-in-renal cell carcinoma” (erc) DCs that were often found in tight contact with dysfunctional T cells. Using transcriptional profiling and flow cytometry, we describe here that ercDCs represent a mosaic cell type within the macrophage continuum co-expressing M1 and M2 markers. The polarization state reflects tissue-specific signals that are characteristic of RCC and renal tissue homeostasis. ErcDCs are tissue-resident with increasing prevalence related to tumor grade. Accordingly, a high ercDC score predicted poor patient survival. Within the profile, therapeutic targets (VSIG4, NRP1, GPNMB) were identified with promise to improve immunotherapy.

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Publication type Article: Journal article

Document type Scientific Article

Corresponding Author

Keywords Gene Expression ; Gpnmb ; Macrophage Plasticity ; Mononuclear Phagocyte System ; Nrp1 ; Tissue Macrophage ; Tumor Microenvironment ; Vsig4

ISSN (print) / ISBN 2073-4409

e-ISSN 2073-4409

Journal Cells

Quellenangaben Volume: 11, Issue: 20, Article Number: 3289

Publisher MDPI

Publishing Place Basel

Non-patent literature Publications

Institute(s) CF Immunoanalytics (IMA)
Institute of Experimental Genetics (IEG)

Grants Deutsche Krebshilfe
Deutsche Forschungsgemeinschaft
Robert Bosch Stiftung
ICEPHA Graduate School Tuebingen-Stuttgart
Helmholtz Alliance