Influence of Environmental Exposures on the Development and Function of the Immune System
Our research focuses on understanding how the environment influences overall health, with a particular focus on the immune system. We define ‘environment’ very broadly. As such, past, current, and potential future research questions consider pollutants, natural products and therapeutic agents under the umbrella of ‘environment.’ Some of our investigative efforts seek to define, at the cellular and molecular level, precisely how environmental exposures modify the function of the immune system. For much of this research we probe the integrated function of the immune system using infectious agents, such as influenza viruses. However, past and on-going projects include the use of a variety of immune triggers, including models of allergic asthma and autoimmune diseases.
Other research centers on delineating how exposure during a critical period of development, such as in utero or immediately after birth, change the functional capacity of the immune system and impact health later in life. This research includes experiments to identify how environmental signals alter epigenetic regulatory mechanisms in the cells of the immune system, as they are developing, and how these modifications change immune system function and alter disease processes later in life.
To conduct our research, we integrate many approaches, including mouse genetics, pharmacological and biochemical modifiers of cellular processes, numerous immunological tools, gene-specific and genome-wide analyses, and state-of-the art multi-color flow cytometry.
Current Research Projects
- Developmental Activation of the AHR Increases Effector CD4+ T Cells and Exacerbates Symptoms in Autoimmune Disease-Prone Gnaq+/- Mice.Toxicol Sci. 148, 555-66. (2015 Dec 01).
- Activation of the aryl hydrocarbon receptor during development enhances the pulmonary CD4+ T-cell response to viral infection.Am J Physiol Lung Cell Mol Physiol. 309, L305-13. (2015 Aug 01).
- Linking the aryl hydrocarbon receptor with altered DNA methylation patterns and developmentally induced aberrant antiviral CD8+ T cell responses.J Immunol. 194, 4446-57. (2015 May 01).