Allergic inflammation (AI) is a reaction that occurs in diseases such as asthma, atopic dermatitis, and food allergy. In genetically predisposed (atopic) subjects, repeated allergen exposure can lead to chronic AI, which is still an important unmet clinical need. Therefore, it is most important to develop new therapeutical strategies against allergic inflammation, involving for example inhibitory receptors (IRs) and resolution pathways.
Part of my research focuses on the inhibitory receptor CD300a and its role in resolution of inflammation. The particularity of this receptor lies in its ability to bind lipids, especially phosphatidylserine expressed on the membrane of activated or apoptotic cells. The hypothesis is that modulation of this receptor, as expressed by the cardinal cells of allergy, mast cells and esoinophils, might positively influence the course of inflammation. This study involves the use of CD300a KO mice.
Secondly, I study the pro-resolutory lipid mediators Resolvin D1 and Lipoxin A4, their effect on and their production from mast cells and eosinophils and their co-culture. Preliminary results show that these molecules, once bound to their surface receptors, can decrease the inflammatory signals and production of pro-inflammatory mediators.
Ongoing projects are focusing on investigating whether mast cells might have a pro-resolutory role in AI in vitro and in vivo.
This research is conducted in collaboration with Bruce D. Levy’s laboratory at the Brigham and Women’s Hospital, Harvard Medical School, Boston.