NDLI: Cross-presenting human γδ T cells induce robust CD8+ αβ T cell responses

Content Provider	PubMed Central
Author	Brandes, Marlène Willimann, Katharina Gilles, Bioley Lévy, Nicole Eberl, Matthias Luo, Ming Robert, Tampé Lévy, Frédéric Romero, Pedro Moser, Bernhard
Abstract	γδ T cells are implicated in host defense against microbes and tumors but their mode of function remains largely unresolved. Here, we have investigated the ability of activated human Vγ9Vδ2+ T cells (termed γδ T-APCs) to cross-present microbial and tumor antigens to CD8+ αβ T cells. Although this process is thought to be mediated best by DCs, adoptive transfer of ex vivo antigen-loaded, human DCs during immunotherapy of cancer patients has shown limited success. We report that γδ T-APCs take up and process soluble proteins and induce proliferation, target cell killing and cytokine production responses in antigen-experienced and naïve CD8+ αβ T cells. Induction of APC functions in Vγ9Vδ2+ T cells was accompanied by the up-regulation of costimulatory and MHC class I molecules. In contrast, the functional predominance of the immunoproteasome was a characteristic of γδ T cells irrespective of their state of activation. γδ T-APCs were more efficient in antigen cross-presentation than monocyte-derived DCs, which is in contrast to the strong induction of CD4+ αβ T cell responses by both types of APCs. Our study reveals unexpected properties of human γδ T-APCs in the induction of CD8+ αβ T effector cells, and justifies their further exploration in immunotherapy research.
Related Links	http://dx.doi.org/10.1073/pnas.0810059106
Ending Page	2312
Page Count	6
Starting Page	2307
File Format	PDF
ISSN	00278424
e-ISSN	10916490
Journal	Proceedings of the National Academy of Sciences of the United States of America
Issue Number	7
Volume Number	106
Language	English
Publisher	National Academy of Sciences
Publisher Date	2009-02-17
Access Restriction	Open
Rights Holder	National Academy of Sciences
Subject Keyword	General Research in Higher Education
Content Type	Text
Resource Type	Article
Subject	Multidisciplinary

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