Potential for Collaboration
Epidemiologists and Clinicians, Biochemists and Chemists
It is often difficult to prove whether or not a particular environmental factor, such as a pollutant, causes or exacerbates a specific disease. One reason for this difficulty is that rarely is information gathered to determine how much of a particular chemical an individual or group of people has been exposed to. Few studies are designed to assess a particular health outcome from a specific exposure in large groups of people over long periods of time. Furthermore, when we study people, we often only have access to their medical records and maybe blood samples. However, when our body fights an infection or someone has a disease caused by deregulation of their immune system, the relevant place to look at what is going on is frequently not the blood, but an organ within the body. These complications make it difficult to measure changes to immune function in people, and lead to gaps in our understanding of the effects of these toxins. Partnership between epidemiologists, clinicians, biochemists and immunologists will help us better resolve these unknowns, and make advancements toward better understanding the contribution of environmental exposures to human health and disease.
Pharmacologists and Clinicians
It was recently discovered that some naturally derived products, such as compounds in foods we eat, as well as possible new drugs work through the AhR to modify immune responses. This discovery means that it may be possible to develop more effective and less toxic immunotherapies to help the body fight off infections, or to treat allergic and autoimmune diseases. But, in order to use AhR as an effective target for immunotherapy, there needs to be a better understanding of how the many chemicals that bind to it alter the function of the immune system. There also needs to be a means of testing possible disease treatments in relevant model systems. Partnership with pharmacologists and clinicians would be advantageous to the development and testing of potential immune treatments that work through the AhR.
- 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).
- Influenza A virus-dependent remodeling of pulmonary clock function in a mouse model of COPD.Sci Rep. 4, 9927. (2015 Jan 01).