High fat diet and leptin promote tumor progression by inducing myeloid-derived suppressor cells

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dc.contributor.authorClements, Virginia K.
dc.contributor.authorLong, Tiha
dc.contributor.authorLong, Ramses
dc.contributor.authorFigley, Chas
dc.contributor.authorSmith, Daniel
dc.contributor.authorOstrand-Rosenberg, Suzanne
dc.date.accessioned2018-04-19T12:40:19Z
dc.date.available2018-04-19T12:40:19Z
dc.date.issued2018
dc.description"This is the pre-peer reviewed version of the following article: Clements, V.K., Long, T., Long, R., Figley, C., Smith, D.M.C., Ostrand-Rosenberg, S., 2018. Frontline Science: High fat diet and leptin promote tumor progression by inducing myeloid-derived suppressor cells. J. Leukoc. Biol. 103:395-407. , which has been published in final form at doi:10.13016/M2Z02ZB5K. This article may be used for non-commercial purposes in accordance with Wiley Terms and Conditions for Self-Archiving."
dc.description.abstractObesity is a risk factor for cancer incidence and cancer mortality. The association of obesity and cancer is attributed to multiple factors, but the tightest linkage is with the chronic, low‐grade inflammation that accompanies obesity. Myeloid‐derived suppressor cells (MDSC) are known facilitators of cancer progression that act by suppressing the activation and function of tumor‐reactive T cells. Because MDSC quantity and function are driven by chronic inflammation, we hypothesized that MDSC may accumulate in obese individuals and facilitate tumor growth by suppressing antitumor immunity. To test this hypothesis, tumor‐bearing mice on a high fat or low fat diet (HFD or LFD) were assessed for tumor progression and the metabolic dysfunction associated with obesity. HFD enhanced the accumulation of MDSC, and the resulting MDSC had both beneficial and detrimental effects. HFD‐induced MDSC protected mice against diet‐induced metabolic dysfunction and reduced HFD‐associated inflammation, but also increased the accumulation of fat, enhanced tumor progression, and spontaneous metastasis and reduced survival time. HFD‐induced MDSC facilitated tumor growth by limiting the activation of tumor‐reactive CD8+ T cells. Leptin, an adipokine that regulates appetite satiety and is overexpressed in obesity, undergoes crosstalk with MDSC in which leptin drives the accumulation of MDSC while MDSC down‐regulate the production of leptin. Collectively, these studies demonstrate that although MDSC protect against some metabolic dysfunction associated with HFD they enhance tumor growth in HFD mice and that leptin is a key regulator linking HFD, chronic inflammation, immune suppression, and tumor progression.en_US
dc.description.urihttps://doi.org/10.1002/JLB.4HI0517-210Ren_US
dc.format.extent46 pagesen_US
dc.genrejournal articlesen_US
dc.identifierdoi:10.13016/M2Z02ZB5K
dc.identifier.citationClements, V.K., Long, T., Long, R., Figley, C., Smith, D.M.C., Ostrand-Rosenberg, S., 2018. Frontline Science: High fat diet and leptin promote tumor progression by inducing myeloid-derived suppressor cells. J. Leukoc. Biol. 103:395-407. (en_US
dc.identifier.urihttp://hdl.handle.net/11603/8779
dc.language.isoen_USen_US
dc.publisherWileyen_US
dc.relation.isAvailableAtThe University of Maryland, Baltimore County (UMBC)
dc.relation.ispartofUMBC Biological Sciences Department Collection
dc.relation.ispartofUMBC Faculty Collection
dc.rightsThis item may be protected under Title 17 of the U.S. Copyright Law. It is made available by UMBC for non-commercial research and education. For permission to publish or reproduce, please contact the author.
dc.subjectobesityen_US
dc.subjectinflammationen_US
dc.subjectimmune supressionen_US
dc.subjectprogrammed death ligand 1en_US
dc.titleHigh fat diet and leptin promote tumor progression by inducing myeloid-derived suppressor cellsen_US
dc.typeTexten_US

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