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Myeloid molecular characteristics of human γδ T cells support their acquisition of tumor antigen-presenting capacity

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Title: Myeloid molecular characteristics of human γδ T cells support their acquisition of tumor antigen-presenting capacity
Authors: Muto, Masato Browse this author
Baghdadi, Muhammad Browse this author
Maekawa, Ryuji Browse this author
Wada, Haruka Browse this author →KAKEN DB
Seino, Ken-ichiro Browse this author →KAKEN DB
Keywords: γδ T cells
Antigen-presenting capacity
Issue Date: Aug-2015
Publisher: Springer
Journal Title: Cancer immunology, immunotherapy
Volume: 64
Issue: 8
Start Page: 941
End Page: 949
Publisher DOI: 10.1007/s00262-015-1700-x
PMID: 25904200
Abstract: Human T cells expressing γδ T cell receptor have a potential to show antigen-presenting cell-like phenotype and function upon their activation. However, the mechanisms that underlie the alterations in human γδ T cells remain largely unclear. In this study, we have investigated the molecular characteristics of human γδ T cells related to their acquisition of antigen-presenting capacity in comparison with activated αβ T cells. We found that activated γδ but not αβ T cells upregulated cell surface expression of a scavenger receptor, CD36, which seemed to be mediated by signaling through mitogen-activated protein kinase and/or NF-κB pathways. Confocal microscopical analysis revealed that activated γδ T cells can phagocytose protein antigens. Activated γδ T cells could induce tumor antigen-specific CD8+ T cells using both apoptotic and live tumor cells as antigen resources. Furthermore, we detected that C/EBPα, a critical transcription factor for the development of myeloid-lineage cells, is expressed much higher in γδ T cells than in αβ T cells. These results unveiled the molecular mechanisms for the elicitation of antigen-presenting functions in γδ T cells and would also help designing new approaches for γδ T cell-mediated human cancer immunotherapy.
Rights: The final publication is available at Springer via
Type: article (author version)
Appears in Collections:遺伝子病制御研究所 (Institute for Genetic Medicine) > 雑誌発表論文等 (Peer-reviewed Journal Articles, etc)

Submitter: 清野 研一郎

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