Nicola Heller, Ph.D.
Key words: interleukin(IL)-4/IL-13 signaling, allergic inflammation, asthma, IRS-2, STAT6, alternatively activated macrophage.
We are interested in the basic mechanisms of signaling from the biology of the IL-4/IL-13 receptor, signal transduction and its regulation to the role of alternatively-activated macrophages (AAM) in the pathogenesis of allergic inflammation. IL-4 and/or IL-13 are critical for AAM differentiation from resting macrophages. AAM mediate Th2-type inflammatory responses (to allergens or helminths) and wound healing responses. AAM are considered “anti-inflammatory” and suppress inflammation by promoting fibrosis through release of chitinase-like molecules and matrix remodeling enzymes, inducing Tregs, dampening T-cell responses and producing anti-inflammatory cytokines. However, when AAM responses become chronic or are dysregulated, pathogenesis can result, as seen in lung fibrosis and tissue remodeling in asthma. The balance between AAM and classical inflammatory macrophages regulates the pathology of many diseases including obesity, cardiovascular disease and cancer. New projects include elucidating the molecular links between asthma and obesity and how gender and race affect asthma and obesity in humans.
Publications and Interests: https://jhu.pure.elsevier.com/en/persons/nicola-mary-heller