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Yuzhu Hou

Researcher at University of Chicago

Publications -  27
Citations -  1248

Yuzhu Hou is an academic researcher from University of Chicago. The author has contributed to research in topics: Medicine & Immune system. The author has an hindex of 12, co-authored 17 publications receiving 748 citations. Previous affiliations of Yuzhu Hou include Chinese Academy of Sciences & Xi'an Jiaotong University.

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Host STING-dependent MDSC mobilization drives extrinsic radiation resistance

TL;DR: It is proposed that radiation-induced STING activation is immunosuppressive due to (monocytic) M-MDSC infiltration, which results in tumor radioresistance and can be abrogated in humans by a translational strategy involving anti-CCR2 antibody treatment to improve radiotherapy.
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TSC1 controls macrophage polarization to prevent inflammatory disease

TL;DR: It is shown that tuberous sclerosis complex 1 (TSC1) is a critical regulator of M1 and M2 phenotypes of macrophages and a key role for TSC1 in orchestrating macrophage polarization via mTOR-dependent and independent pathways.
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Tumor-reprogrammed resident T cells resist radiation to control tumors.

TL;DR: It is shown that unlike circulating lymphocytes, tumor-infiltrating T cells survive therapeutic doses of irradiation, remaining functional and contributing to radiotherapy induced anti-tumor immunity.
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Non-canonical NF-κB Antagonizes STING Sensor-Mediated DNA Sensing in Radiotherapy

TL;DR: It is demonstrated that inhibiting the canonical NF‐&kgr;B pathway dampened the therapeutic effect of ionizing radiation (IR), whereas non‐canonical NF-B deficiency promoted IR‐induced anti‐tumor immunity.
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IL-23-induced macrophage polarization and its pathological roles in mice with imiquimod-induced psoriasis

TL;DR: A unique pathogenic macrophage subpopulation driven by IL-23 with a distinct gene expression profile including defined types of cytokines is identified, significantly promote the dermatitis pathogenesis in a psoriasis-like mouse model and may help understand the contribution of macrophages subpopulation in Th17-cytokines-related pathogenesis.