Non-oncogenic Acute Viral Infections Disrupt Anti-cancer Responses and Lead to Accelerated Cancer-Specific Host Death. |
Authors: |
Kohlhapp, Frederick J Huelsmann, Erica J Lacek, Andrew T Schenkel, Jason M Lusciks, Jevgenijs Broucek, Joseph R Goldufsky, Josef W Hughes, Tasha Zayas, Janet P Dolubizno, Hubert Sowell, Ryan T Kühner, Regina Burd, Sarah Kubasiak, John C Nabatiyan, Arman Marshall, Sh'Rae Bommareddy, Praveen K Li, Shengguo Newman, Jenna H Monken, Claude E Shafikhani, Sasha H Marzo, Amanda L Guevara-Patino, Jose A Lasfar, Ahmed Thomas, Paul G Lattime, Edmund C Kaufman, Howard L Zloza, Andrew
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Citation: |
Kohlhapp FJ, etal., Cell Rep. 2016 Oct 18;17(4):957-965. doi: 10.1016/j.celrep.2016.09.068. |
RGD ID: |
40818261 |
Pubmed: |
PMID:27760326 (View Abstract at PubMed) |
PMCID: |
PMC5589518 (View Article at PubMed Central) |
DOI: |
DOI:10.1016/j.celrep.2016.09.068 (Journal Full-text) |
In light of increased cancer prevalence and cancer-specific deaths in patients with infections, we investigated whether infections alter anti-tumor immune responses. We report that acute influenza infection of the lung promotes distal melanoma growth in the dermis and leads to accelerated cancer-specific host death. Furthermore, we show that during influenza infection, anti-melanoma CD8+ T cells are shunted from the tumor to the infection site, where they express high levels of the inhibitory receptor programmed cell death protein 1 (PD-1). Immunotherapy to block PD-1 reverses this loss of anti-tumor CD8+ T cells from the tumor and decreases infection-induced tumor growth. Our findings show that acute non-oncogenic infection can promote cancer growth, raising concerns regarding acute viral illness sequelae. They also suggest an unexpected role for PD-1 blockade in cancer immunotherapy and provide insight into the immune response when faced with concomitant challenges.
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Genes (Rattus norvegicus) |
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Pdcd1 (programmed cell death 1) |
Genes (Mus musculus) |
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Pdcd1 (programmed cell death 1) |
Genes (Homo sapiens) |
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PDCD1 (programmed cell death 1) |
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