ORCID Profile
0000-0003-1438-0772
Current Organisations
University of Queensland
,
Monash University
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Publisher: University of Queensland Library
Date: 2019
Publisher: Springer Science and Business Media LLC
Date: 31-07-2017
DOI: 10.1038/NI.3800
Abstract: Avoiding destruction by immune cells is a hallmark of cancer, yet how tumors ultimately evade control by natural killer (NK) cells remains incompletely defined. Using global transcriptomic and flow-cytometry analyses and genetically engineered mouse models, we identified the cytokine-TGF-β-signaling-dependent conversion of NK cells (CD49a
Publisher: Elsevier BV
Date: 02-2019
DOI: 10.1016/J.SMIM.2019.04.001
Abstract: The advance of immunotherapies has revolutionized the treatment of cancer patients. Mostly agents modulating the adaptive immune system are currently used. More recently, attempts to stimulate the innate immune system are being promoted for clinical evaluation. Innate lymphoid cells (ILCs) are a highly plastic population of immune cells crucial for tissue homeostasis and the regulation of immune responses and maybe a promising target to improve current cancer immunotherapies. Although we have made significant progress in understanding ILC biology, their impact on tumor development, progression and therapy is controversial. In this review, we discuss the recent advances of ILC function and plasticity in the context of cancer.
Publisher: Elsevier BV
Date: 10-2014
DOI: 10.1016/J.CCR.2014.07.026
Abstract: Epstein-Barr virus-induced lymphoproliferative disease (EBV-LPD) after transplantation remains a serious and life-threatening complication. Herein we showed that the aminobisphosphonate pamidronate-expanded human Vγ9Vδ2-T cells efficiently killed EBV-transformed autologous lymphoblastoid B cell lines (EBV-LCL) through γ/δ-TCR and NKG2D receptor triggering and Fas and TRAIL engagement. By inoculation of EBV-LCL in Rag2(-/-)γc(-/-) mice and humanized mice, we established lethal EBV-LPD with characteristics close to those of the human disease. Adoptive transfer of pamidronate-expanded Vγ9Vδ2-T cells alone effectively prevented EBV-LPD in Rag2(-/-)γc(-/-) mice and induced EBV-LPD regression in EBV(+) tumor-bearing Rag2(-/-)γc(-/-) mice. Pamidronate treatment inhibited EBV-LPD development in humanized mice through selective activation and expansion of Vγ9Vδ2-T cells. This study provides proof-of-principle for a therapeutic approach using pamidronate to control EBV-LPD through Vγ9Vδ2-T cell targeting.
Publisher: American Association for Cancer Research (AACR)
Date: 14-02-2017
DOI: 10.1158/0008-5472.CAN-17-2826
Abstract: Extracellular adenosine is a key immunosuppressive metabolite that restricts activation of cytotoxic lymphocytes and impairs antitumor immune responses. Here, we show that engagement of A2A adenosine receptor (A2AR) acts as a checkpoint that limits the maturation of natural killer (NK) cells. Both global and NK-cell–specific conditional deletion of A2AR enhanced proportions of terminally mature NK cells at homeostasis, following reconstitution, and in the tumor microenvironment. Notably, A2AR-deficient, terminally mature NK cells retained proliferative capacity and exhibited heightened reconstitution in competitive transfer assays. Moreover, targeting A2AR specifically on NK cells also improved tumor control and delayed tumor initiation. Taken together, our results establish A2AR-mediated adenosine signaling as an intrinsic negative regulator of NK-cell maturation and antitumor immune responses. On the basis of these findings, we propose that administering A2AR antagonists concurrently with NK cell–based therapies may heighten therapeutic benefits by augmenting NK cell–mediated antitumor immunity. Significance: Ablating adenosine signaling is found to promote natural killer cell maturation and antitumor immunity and reduce tumor growth. Cancer Res 78(4) 1003–16. ©2017 AACR.
Publisher: Wiley
Date: 2018
DOI: 10.1002/CTI2.1003
No related grants have been discovered for Yulong Gao.