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Thomas Rogers, PhD

Director and Professor, Center for Inflammation and Lung Research
Professor, Microbiology, Immunology and Inflammation
Professor, Center for Substance Abuse Research
Professor, Fels Cancer Institute for Personalized Medicine

Thomas Rogers
Contact Information

Contact Information




About Me

Research Interests

Our basic research interests have centered on an understanding of the cross-talk between G protein-coupled receptors (GPCRs) at the level of both protein function and gene expression.

We have focused our attention on chemokine, opioid, and formyl peptide receptors because these groups of receptors play a significant role in the regulation of inflammatory responses: first, the capacity of these receptors to regulate the expression other GPCRs and their cognate ligands; and secondthe cross-talk between opioid and chemokine receptors at the level of protein function.

Our studies show that activation of certain GPCRs induces the expression of several chemokines and chemokine receptors, including those chemokines that perform critical pro-inflammatory functions. In contrast, there is a category of GPCRs which mediates anti-inflammatory responses by directly inhibiting the expression of pro-inflammatory chemokines and/or their receptors. 

We have found that several GPCRs are capable of the cross-regulation of other GPCRs through a process termed “heterologous desensitization." This process occurs when one GPCR is activated by its ligand and induces a signaling pathway which leads to the inactivation of a second, and distinct, GPCR.

Our current work suggests that it should be possible to utilize the process of heterologous desensitization to devise strategies to develop treatment therapies for a number of important disease states.

We are also actively engaged in studies to examine the basis for the development and progression of COPD. Our studies have shown that patients with severe forms of this disease develop an unusual inflammatory disease pattern which results in much greater accumulation of aggressive inflammatory cells in the lung tissue. The mechanisms responsible for this form of immunological dysfunction are the subject of our current research work.

Education, Training & Credentials

Educational Background

  • PhD, University of Wisconsin, Madison

Digital Bibliography

View PubMed Publications

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