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Andrew L. Doedens

Researcher at University of California, San Diego

Publications -  25
Citations -  4830

Andrew L. Doedens is an academic researcher from University of California, San Diego. The author has contributed to research in topics: Cytotoxic T cell & CD8. The author has an hindex of 20, co-authored 25 publications receiving 4104 citations. Previous affiliations of Andrew L. Doedens include Indiana University & University of Edinburgh.

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HIF-1α expression regulates the bactericidal capacity of phagocytes

TL;DR: HIF-1alpha was induced by bacterial infection, even under normoxia, and regulated the production of key immune effector molecules, including granule proteases, antimicrobial peptides, nitric oxide, and TNF-alpha.
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Macrophage Expression of Hypoxia-Inducible Factor-1α Suppresses T-Cell Function and Promotes Tumor Progression

TL;DR: It is found that hypoxia powerfully augmented macrophage-mediated T-cell suppression in vitro in a manner dependent on macrophages expression of HIF-1α, which links the innate immune hypoxic response to tumor progression through induction of T- cell suppression in the tumor microenvironment.
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Differential activation and antagonistic function of HIF-α isoforms in macrophages are essential for NO homeostasis

TL;DR: The studies reveal that the two homologous transcription factors, Hif-1alpha and HIF-2alpha, can have physiologically antagonistic functions, but that their antiphase regulation allows them to coordinately regulate NO production in a cytokine-induced and transcription-dependent fashion.
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Hypoxia-inducible factors enhance the effector responses of CD8 + T cells to persistent antigen

TL;DR: It is found that HIFs and oxygen influenced the expression of pivotal transcription, effector and costimulatory-inhibitory molecules of CTLs, which was relevant to strategies that promote the clearance of viruses and tumors.
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Deletion of vascular endothelial growth factor in myeloid cells accelerates tumorigenesis

TL;DR: Deletion of myeloid-cell VEGF-A resulted in an accelerated tumour progression in multiple subcutaneous isograft models and an autochthonous transgenic model of mammary tumorigenesis, with less overall tumour cell death and decreased tumour hypoxia.