Yongxia Wu, MD, PhD
Research Assistant Professor
Locations
- B2230
Contact Information
General Interests
Hematopoietic Stem Cell Transplantation, Graft-versus-Host Disease, Graft-versus-Leukemia Effect, Cancer Immunotherapy
Education
PhD, Hematology, Capital Medical University, Beijing, China, 2015
MD, Clinical Medicine, Shandong University, Jinan, Shandong, China, 2010
MD, Clinical Medicine, Shandong University, Jinan, Shandong, China, 2010
Research Interests
Research Areas of Interest:
T-Lymphocytes, Antigen-Presenting Cells, Adoptive Cell Therapy, Acute and Chronic Graft-versus-Host Disease, Graft-versus-Leukemia Effect, Non-Coding RNAs
Research Experience:
Mice, Bone Marrow Transplantation, Adoptive T-cell Therapy, Cell Isolation and Purification, Cell Proliferation and Differentiation, Mixed Lymphocyte Reaction, Treg Generation, Flow Cytometry, Metabolic Analysis
My research interests include:
- Understand biology of lymphocytes and antigen-presenting cells in graft-versus-host disease (GVHD) and graft-versus-leukemia (GVL) effect.
Our goal is to find therapeutic targets to improve allogeneic hematopoietic stem-cell transplantation (HCT) by attenuating GVHD while sparing GVL activity. One of my interested areas is to define immune microRNAs (miRNAs) that regulate T- and B-cell pathogenicity in acute and chronic GVHD. Our recent studies provide preclinical evidence that miRNAs play an essential role in T- and B-cell pathogenicity in GVHD, and that pharmacological inhibition of specific miRNAs represents a potential strategy for controlling acute and chronic GVHD.
- Improve cancer immunotherapy by increasing longevity and activity of T cells in adoptive cell therapy.
Our recent study found a novel and critical role of protein kinase PIM-2 in T-cell mediated GVL and anti-solid tumor response. PIM-2 isoform negatively regulated T cell responses as T cells deficient in PIM-2 resulted in dramatically accelerated GVHD severity after allogeneic HCT and substantially enhanced antitumor response in adoptive T cell immunotherapy. We will define molecular mechanism how PIM-2 inhibits metabolism and fitness of T cells, and further illustrate a key role of PIM-2 in suppressing T cell responses that will provide a strong rationale to target PIM-2 for cancer immunotherapy, including CAR-T therapy for hematological malignancy.