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Jiajun (Brian) Zhou

Jiajun ZhouCooperating Doctoral Program: Microbiology and Molecular Genetics

EITS Track: Biomedical Toxicology

Education: B.S., Biochemistry and Molecular Biology / Microbiology, Michigan State University

Research Interests:
Suppression of antibody response by 2,3,7,8-tetrachlorodiobenzo-p-dioxin (TCDD) has been observed in variety of species. However, the molecular mechanism of TCDD mediated AHR activation on antibody suppression in human primary B cells has not been fully understood. To address this question, a Lentiviral construct containing a dioxin responsive element (DRE)-driven GFP is created and transduced to human primary B cells to quantify the activation of AHR. In a 4-day (0, 24, 48, 72, 96h) model, B cells are activated with irradiated CD40L expressing fibroblast cell line (CD40L-L cells) with cytokines (IL-2, IL-6 and IL-10) in the absence or present of TCDD (0.1, 1, 10 and 30 nM). Cells will be stained and analyzed for viability, GFP, CD80, CD86 and CD69. The alteration of cell surface activation marker and cellular viability could be used to correlate to the magnitude of responsiveness of B cells to TCDD in the context of DRE-driven GFP expression. Similar model system can be used to determine the intracellular markers known to be the downstream regulators of B cell activation. At all time-point, B cells will be stained for intracellular pERK, p-AKT, p-p65 and pSTAT3. The magnitude of AHR activation by TCDD (expression of GFP) can be correlated with the alteration of intercellular markers in B cells. The advantage of using these experimental models is to quantify the magnitude of AHR activation and to correlate with the molecular changes in single B cell level, which provides further understanding of the mechanism of
TCDD-mediated antibody suppression.

Major Professor: Norbert Kaminski, Pharmacology and Toxicology