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Ye Zheng

Ye Zheng

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Ye Zheng is associate professor in the NOMIS Center for Immunobiology and Microbial Pathogenesis at the Salk Institute for Biological Studies (US).

Zheng received a BS in biochemistry and molecular biology from Peking University (China) and a PhD from Columbia University (US). He was a postdoctoral fellow at the University of Washington (US) and a research scholar at Memorial Sloan-Kettering Cancer Center. He completed a postdoctoral fellowship at the Cancer Research Institute from 2005-2008 and was a Rita Allen Foundation Scholar from 2010-2015.

Zheng’s research focuses on a specialized set of immune cells called regulatory T cells (Tregs) that act to balance and maintain a healthy immune system. Tregs control the immune response, telling the more aggressive immune cells when to stop their frenzied attack. Abnormal Treg function has been linked to a number of autoimmune diseases, such as arthritis, type 1 diabetes, lupus and multiple sclerosis. A key molecular component of these cells, a protein called Foxp3, is often responsible for deficient Tregs. Zheng is making advances in understanding the genes that control Foxp3—as well as genes that Foxp3 controls—to ultimately lead to ways to manage Treg function. Since manipulations of Tregs can either weaken or strengthen the immune response, his findings can potentially open new avenues in the treatment of autoimmune diseases, improve organ transplant survival and uncover new cancer targets.

Ye Zheng | Awards Film

Ye Zheng | Insights Film

Ye Zheng's News

In a conversation with Inside Salk, Ye Zhen, associate professor at the NOMIS Foundation Laboratories for Immunbiology and Microbial Pathogenesis, shares his hopes and his hesitations about tapping our immune […]

Ye Zheng's Insights

Abstract: The limited efficacy of immunotherapies against glioblastoma underscores the urgency of better understanding immunity in the central nervous system. We found that treatment with αCTLA-4, but not αPD-1, prolonged survival in a mouse model of mesenchymal-like glioblastoma. This effect was lost upon the depletion of CD4+ T cells but not
Abstract: Retinoid-related orphan receptor (RAR) gamma (RORγt)-expressing regulatory T cells (RORγt+ Tregs) play pivotal roles in preventing T cell hyperactivation and maintaining tissue homeostasis, in part by secreting the anti-inflammation cytokine interleukin-10 (IL-10). Here, we report that hypoxia-induced factor 1α (HIF1α) is the master transcription factor for Il10 in RORγt+ Tregs.