Digestive Health Center

  • Chronic Liver Disease

    Mohamed Shata, MD, PhD
    Associate Professor
    Department of Internal Medicine; Division of Digestive Diseases

    Description of Research

    Dr. Shata studies the cellular immune responses to Hepatitis E (HEV), using samples from patients with chronic liver disease in the local area and from an endemic area in Egypt. Additionally, he works in collaboration with Dr. Sherman to develop and perform a clinical intervention trial in hepatitis C virus/human immunodeficiency virus (HCV/HCV) co-infected subjects treated with antiretroviral therapy in order to characterize early/late HCV and HIV viral kinetics. His laboratory evaluates the HCV-specific immune responses in HIV/HCV coinfected patients during therapy and identifies the mechanisms of HCV rebound during antiretroviral therapy. Furthermore, Dr. Shata’s laboratory has developed a system to isolate and characterize Th17 in vitro. He uses this system to examine the role of Th17 in patients with inflammatory bowel disease (IBD). Specifically, Dr. Shata is identifying the cytokine profiles and the roles of IL-17 as well as IL-22 secreting T cells in IBD patients. Dr. Shata is also exploring the role of gut-associated Th17 in microbial translocation in HIV and HCV/HIV coinfected patients.  

    Collaborations and Core Use

    Dr. Shata works with Drs. Blackard and Sherman to evaluate the Hepatitis C Virus (HCV) specific immune responses in HIV/HCV co-infected patients during therapy and identify the mechanisms of HCV rebound during antiretroviral therapy. Projection of Core use: Gene and Protein Expression and Integrative Morphology Cores.

 
  • Research image.

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    Research image.
    Response of human CD4+ IL-23R+ cells stimulated with anti-CD3/CD28 in the presence of different cytokines in the culture media. Data were calculated as the responses in the presence of cytokines and anti-CD3/CD28 beads divided by the responses in the absence of cytokines and anti-CD3/CD28 beads. IL-2, IL-7, IL-12, and IL-12 plus IL-7 significantly increased IFN-γ secretion compared to the level for nonstimulated cells. Additionally, IL-7, IL-12, and IL-12 plus IL-7 significantly increased IL-17 secretion compared to the level for nonstimulated cells. Figure from Clin Vaccine Immunol, 2009; 16: 798–805