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I’ve been focusing on PD-1/PD-L1 co-inhibitory pathway and Th17 cells in patients with HBV-related hepatocellular carcinoma. My work found that both PD-1 (expressed on CD8+ and CD4+T cells) and its ligand, PD-L1 (on tumor cells) expressions played an pivotal role in immune evasion, by inducing the tolerance of CD8+T and Th17 cells, inhibiting their infiltration and triggering their apoptosis by PD-1/PD-L1 pathway. Although tumor microenvironment favored Th17 differentiation, PD-1/PD-L1 pathway constrained Th17-associated inflammation to a much milder and gentler degree, which in the opposite would promote tumor growth. Both works elucidated the regulatory mechanisms in tumor microenvironment in human. Besides, I’m also working with the humanized mouse models to elucidate the underlying mechanisms accounting for lymphoma genesis and to evaluate biologics before clinical trials. Until now, two humanized mouse models, one for follicular lymphoma (indolent) and the other for diffuse large B-cell lymphoma (aggressive) lymphoma (DLBCL), are successfully established on my hand, which could be great of use for testing and identifying potential therapeutic targets and novel treatments.
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