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Jing Hong Wang, M.D., Ph.D.

Associate Professor of Immunology & Microbiology

12800 E. 19th Ave., RC1N-9100
Mail Stop 8333, Aurora, CO 80045

Phone: 303-724-8673
Lab: 303-724-8704

Molecular mechanism of somatic hypermutation and class switch recombination: More than 90% of human lymphomas are B cell-derived. This is likely because B cells extensively shuffle their genomic DNA during immune responses. Upon immunizations or infections, activated B cells undergo somatic hypermutation (SHM) and class switch recombination (CSR). Both SHM and CSR rely on the activity of an enzyme called activation induced deaminase (AID). In activated B lymphocytes, AID causes point mutations in the variable regions of the immunoglobulin (Ig) genes. These mutations cause small changes in the protein sequence of antibodies and lead to increased antibody affinity for specific antigens. AID also induces DSBs in the repetitive switch regions that lie upstream of each constant region exon of the Ig heavy chain locus to mediate CSR.  CSR assigns antigen-appropriate effector functions to antibody molecules and is, therefore, a process important for productive immune responses against pathogens.  One of our research interests is to elucidate the mechanisms regulating the signaling control of CSR process.  B cells express phosphatase and tensin homolog (PTEN) and multiple isoforms of class IA phosphoinositide 3-kinase (PI3K) catalytic subunits, including p110α and p110δ, whose roles in CSR remain unknown or controversial.  Our study reveals that a signaling balance between PTEN and PI3K isoforms is essential to maintain normal CSR.  Furthermore, we discovered an important role of p110α in suppressing CSR and found that AKT is the essential downstream effector kinase of PI3Ks to mediate CSR inhibition.  We also propose to address how antigen receptor and co-receptors on B cells cooperatively regulate CSR via affecting AID expression.  

Mechanisms of Immune Evasion in B cell lymphomas or Head Neck Squamous Carcinomas (HNSCC). The goal of our laboratory is to understand the molecular mechanisms that promote chromosomal translocations and cancer development in B lymphocytes by employing mouse models. In particular, we focus on DNA double strand breaks (DSBs) response factors. These proteins are essential for properly repairing DSBs. In the absence of these factors, DSBs will separate and progress into chromosomal breaks and translocations. We are investigating how these proteins suppress oncogenic translocations or cancer development. In addition, we investigate how the interplay of DNA damages and immune responses regulates the mechanisms of cancer immune evasion. We have established interesting B cell lymphoma and HNSCC models which harbor defects in DNA repair and appear to evade the recognition of CD8 or NK cells. We will employ these unique models to elucidate how defects in DNA damage responses enable cancer cells to evade the recognition of immune systems.



Ph.D. Pathology Program, University of Chicago, Chicago, IL.  Degree was granted in June, 2004.  Thesis Advisor: Dr. Yang-Xin Fu


Master of Science. Graduate Program in Department of Molecular Genetics, Ohio State University, Columbus, OH. Degree was granted in December, 1998.  Advisor: Dr. Berl Oakley


Bachelor of Medicine (equivalent to M.D. in U.S.). Department of Basic Medical Sciences, Beijing Medical University, Beijing, P.R. China. Degree was granted in July, 1996.


​2016.7-present ​Associate Professor, Department of Immunology and Microbiology, University of Colorado School of Medicine


Assistant Professor, Department of Immunology and Microbiology, University of Colorado School of Medicine


Instructor of Pediatrics, Immune Disease Institute, Children’s Hospital Boston, Harvard Medical School. Lab PI: Dr. Frederick W. Alt.


Postdoctoral Research Fellow, Immune Disease Institute, Children’s Hospital Boston, Harvard Medical School. Lab PI: Dr. Frederick W. Alt.


Research Associate, Department of Pathology, University of Chicago.  Lab PI: Dr. Yang-Xin Fu.


2014: AAI 2014Early Career Faculty Travel Award

2012: Outstanding Junior Faculty Award, National Jewish Health

2012-2015: American Society of Hematology (ASH) Scholar Award

2011-2014: Boettcher Foundation Webb-Waring Early Career Investigator Award

2005-2008: Leukemia and Lymphoma Society (LLS) senior fellowship

1996-1997: Distinguished University Fellowship, Ohio State University

1996: GuangHua Scholarship, Beijing Medical University

Zhangguo Chen, Ph.D.
Assistant Research Professor

Xiaoguang Wang, Ph.D.
Postdoctoral Fellow

Nicole Koochi, M.S.
Professional Research Assistant

Stephanie Cung
Student Research Assistant

Postdoctoral fellow position available - please email Dr. Wang for more information.
Rotation inquiry welcomed