Xiufen Chen

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Type I interferon (IFN) production by innate immune cells is critical to prime spontaneous T cell responses against solid tumors. Emerging pre-clinical data suggests that tumor-derived DNA induces potent IFN-b production by activating a cytosolic DNA sensing receptor called STING (Stimulator of Interferon Genes), ultimately resulting in tumor(More)
Our laboratory investigates the immune tolerance mechanisms promoted by acute myeloid leukemia (AML). In a murine AML model, we have observed that leukemia antigen-specific T cells are specifically deleted from the host, presumably following interactions with immature host antigen-presenting cells (APCs). Ongoing work focuses on identifying APC subsets that(More)
Spontaneous T cell responses generated against a variety of solid malignancies are often subverted by immune evasion mechanisms active in the tumor microenviron-ment. In contrast, the mechanisms that regulate T cell activation versus tolerance to hematopoietic malignan-cies, such as acute myeloid leukemia (AML), have not been well-characterized. Our recent(More)
Calreticulin (CRT) is a chaperone protein which normally resides in the endoplasmic reticulum (ER). However , recent studies have demonstrated that pre-apoptotic cancer cells release internalized CRT to their surface prior to death, and this surface exposure of CRT acts as an 'eat-me' signal to local phagocytes. Some che-motherapeutic agents and(More)
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