Combined toll-like receptor 3/7/9 deficiency on host cells results in T-cell-dependent control of tumour growth

Johanna C. Klein, Katrin Moses, Gennadiy Zelinskyy, Simon Sody, Jan Buer, Stephan Lang, Iris Helfrich, Ulf Dittmer, Carsten J. Kirschning and Sven Brandau ()
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Johanna C. Klein: University Hospital Essen, University Duisburg-Essen
Katrin Moses: University Hospital Essen, University Duisburg-Essen
Gennadiy Zelinskyy: Institute of Virology, University Hospital Essen, University Duisburg-Essen
Simon Sody: University Hospital Essen, University Duisburg-Essen
Jan Buer: Institute of Medical Microbiology, University Hospital Essen, University Duisberg-Essen
Stephan Lang: University Hospital Essen, University Duisburg-Essen
Iris Helfrich: German Cancer Consortium (DKTK)
Ulf Dittmer: Institute of Virology, University Hospital Essen, University Duisburg-Essen
Carsten J. Kirschning: Institute of Medical Microbiology, University Hospital Essen, University Duisberg-Essen
Sven Brandau: University Hospital Essen, University Duisburg-Essen

Nature Communications, 2017, vol. 8, issue 1, 1-12

Abstract: Abstract Toll-like receptors (TLRs) are located either on the cell surface or intracellularly in endosomes and their activation normally contributes to the induction of protective immune responses. However, in cancer their activation by endogenous ligands can modulate tumour progression. It is currently unknown how endosomal TLRs regulate endogenous anti-tumour immunity. Here we show that TLR3, 7 and 9 deficiencies on host cells, after initial tumour growth, result in complete tumour regression and induction of anti-tumour immunity. Tumour regression requires the combined absence of all three receptors, is dependent on both CD4 and CD8 T cells and protects the mice from subsequent tumour challenge. While tumours in control mice are infiltrated by higher numbers of regulatory T cells, tumour regression in TLR-deficient mice is paralleled by altered vascular structure and strongly induced influx of cytotoxic and cytokine-producing effector T cells. Thus, endosomal TLRs may represent a molecular link between the inflamed tumour cell phenotype, anti-tumour immunity and the regulation of T-cell activation.

Date: 2017
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DOI: 10.1038/ncomms14600

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