Differences in circulating γδ T cells in patients with primary colon cancer and relation with prognostic factors
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2020
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Public Library of Science
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Andreu-Ballester JC, Galindo-Regal L, Hidalgo-Coloma J, Cuéllar C, García-Ballesteros C, Hurtado C, Uribe N, Del Carmen Martín M, Jiménez AI, López-Chuliá F, Llombart-Cussac A. Differences in circulating γδ T cells in patients with primary colon cancer and relation with prognostic factors. PLoS One. 2020 Dec 16;15(12):e0243545. doi: 10.1371/journal.pone.0243545. PMID: 33326443; PMCID: PMC7743935.
Abstract
Downregulation of the T cell system has been proposed as a mechanism to block immunity in colonic cancer (CC). However, little has been studied about circulating αβ and γδ T cells and their immunological status in newly diagnosed patients. The aim of this study was to characterize the αβ and γδ T cell subsets in peripheral blood of patients with CC matched with healthy volunteers. In this prospective case-control study, blood samples were obtained from 96 patients with newly diagnosed treatment-naïve infiltrating colonic adenocarcinoma and 48 healthy volunteers. Pathological report at surgery was obtained from all CC patients. A significant decrease in CD3+ γδ T cells and CD3+CD8+ γδ T cells (p<0.001) were observed in CC patients. Apoptosis was significantly increased in all conventional and both αβ and γδ T cell subsets in patients with CC vs healthy subjects. γδ T cells were decreased in peripheral blood of patients with microscopic infiltration in tissues, history of cancer and synchronous colon cancer (p < 0.05). IFN-γ was significantly reduced in CC patients compared to controls. Cytotoxic effector γδ T cells TEMRA (CD8 and CD56) are the proportionally most abundant T cells in peripheral blood of CC patients. Patients with CC present a deep downregulation in the systemic T-cell immunity. These variations are evident through all tumor stages and suggest that a deficiency in γδ T cell populations could be preventing control of tumor progression. This fact prove the role of immunomodulation on CC carcinogenesis.