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Chaurio RA, Muñoz LE, Maueröder C, et al. The progression of cell death affects the rejection of allogeneic tumors in immune-competent mice - implications for cancer therapy. Front Immunol. 2014;5:560doi: 10.3389/fimmu.2014.00560.
Chaurio, R. A., Muñoz, L. E., Maueröder, C., Janko, C., Harrer, T., Fürnrohr, B. G., Niederweis, M., Bilyy, R., Schett, G., Herrmann, M., & Berens, C. (2014). The progression of cell death affects the rejection of allogeneic tumors in immune-competent mice - implications for cancer therapy. Frontiers in immunology, 5560. https://doi.org/10.3389/fimmu.2014.00560
Chaurio, Ricardo A, et al. "The progression of cell death affects the rejection of allogeneic tumors in immune-competent mice - implications for cancer therapy." Frontiers in immunology vol. 5 (2014): 560. doi: https://doi.org/10.3389/fimmu.2014.00560
Chaurio RA, Muñoz LE, Maueröder C, Janko C, Harrer T, Fürnrohr BG, Niederweis M, Bilyy R, Schett G, Herrmann M, Berens C. The progression of cell death affects the rejection of allogeneic tumors in immune-competent mice - implications for cancer therapy. Front Immunol. 2014 Nov 11;5:560. doi: 10.3389/fimmu.2014.00560. eCollection 2014. PMID: 25426116; PMCID: PMC4227513.
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Front Immunol. 2014 Nov 11;5:560. doi: 10.3389/fimmu.2014.00560. eCollection 2014.

The progression of cell death affects the rejection of allogeneic tumors in immune-competent mice - implications for cancer therapy.

Frontiers in immunology

Ricardo A Chaurio, Luis E Muñoz, Christian Maueröder, Christina Janko, Thomas Harrer, Barbara G Fürnrohr, Michael Niederweis, Rostyslav Bilyy, Georg Schett, Martin Herrmann, Christian Berens

Affiliations

  1. Department of Internal Medicine 3, Friedrich-Alexander University of Erlangen-Nuremberg , Erlangen , Germany.
  2. Department of Internal Medicine 3, Friedrich-Alexander University of Erlangen-Nuremberg , Erlangen , Germany ; Department of Biology, Friedrich-Alexander University of Erlangen-Nuremberg , Erlangen , Germany.
  3. Department of Otorhinolaryngology, Head and Neck Surgery, Section for Experimental Oncology and Nanomedicine (SEON), University Hospital Erlangen , Erlangen , Germany.
  4. Division of Molecular Immunology, Department of Internal Medicine 3, Friedrich-Alexander University of Erlangen-Nuremberg , Erlangen , Germany ; Division of Biological Chemistry, Medical University Innsbruck , Innsbruck , Austria.
  5. Department of Microbiology and Biochemistry, University of Alabama at Birmingham , Birmingham, AL , USA.
  6. Institute of Cell Biology, National Academy of Sciences of Ukraine , Lviv , Ukraine.
  7. Department of Biology, Friedrich-Alexander University of Erlangen-Nuremberg , Erlangen , Germany.

PMID: 25426116 PMCID: PMC4227513 DOI: 10.3389/fimmu.2014.00560

Abstract

Large amounts of dead and dying cells are produced during cancer therapy and allograft rejection. Depending on the death pathway and stimuli involved, dying cells exhibit diverse features, resulting in defined physiological consequences for the host. It is not fully understood how dying and dead cells modulate the immune response of the host. To address this problem, different death stimuli were studied in B16F10 melanoma cells by regulated inducible transgene expression of the pro-apoptotic active forms of caspase-3 (revCasp-3), Bid (tBid), and the Mycobacterium tuberculosis-necrosis inducing toxin (CpnTCTD). The immune outcome elicited for each death stimulus was assessed by evaluating the allograft rejection of melanoma tumors implanted subcutaneously in BALB/c mice immunized with dying cells. Expression of all proteins efficiently killed cells in vitro (>90%) and displayed distinctive morphological and physiological features as assessed by multiparametric flow cytometry analysis. BALB/c mice immunized with allogeneic dying melanoma cells expressing revCasp-3 or CpnTCTD showed strong rejection of the allogeneic challenge. In contrast, mice immunized with cells dying either after expression of tBid or irradiation with UVB did not, suggesting an immunologically silent cell death. Surprisingly, immunogenic cell death induced by expression of revCasp-3 or CpnTCTD correlated with elevated intracellular reactive oxygen species (ROS) levels at the time point of immunization. Conversely, early mitochondrial dysfunction induced by tBid expression or UVB irradiation accounted for the absence of intracellular ROS accumulation at the time point of immunization. Although ROS inhibition in vitro was not sufficient to abrogate the immunogenicity in our allo-immunization model, we suggest that the point of ROS generation and its intracellular accumulation may be an important factor for its role as damage associated molecular pattern in the development of allogeneic responses.

Keywords: DAMPs; ROS; apoptosis; cancer; caspase-3; immunogenicity; necrosis; tBid

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