Early research from her lab led to the identification of NF-?B as a target for glucocorticoid-mediated repression of gene expression and the discovery of GATA-3 as a master regulator of Th2 cells, which promote allergic diseases including asthma. Her laboratory also identified a key role for Tregs expressing membrane-bound TGF-ß with cross-talk with Notch in promoting immune tolerance in the airways.

The primary goal of Dr. Ray’s current research is to understand the immunological and molecular differences between severe and milder asthma and the mechanisms underlying poor response to corticosteroids in severe disease. A study published recently by her group has demonstrated an
IFN-?/Th1 immune bias in more than 50% of severe asthmatics. This study also utilized a newly developed animal model of severe asthma established in her lab, which can be used to test novel therapeutics for severe asthma. This bedside-bench study identified a detrimental role of IFN-? in downregulating expression of the protease inhibitor, SLPI, in the airways of both humans and mice. In the context of immune tolerance, her recently published study has identified an important role of mitochondrial metabolism in lung dendritic cells in the maintenance of immune tolerance in the airways. Studies in her laboratory employ animal models of disease and human samples, which are analyzed using immunological, molecular, biochemical, physiological and imaging techniques.