“We wanted to understand better how B cells influence atherosclerotic diseases, with the long-term goal of developing novel therapies centered on B cells for this life-threatening condition,” says Steffens, outlining the objectives of her research project. She was particularly interested in the receptor GPR55, which forwards chemical signals from the exterior to the interior of cells.B cells in the spleen of mice produce the molecule in large quantities. For their study, the scientists investigated mouse models for atherosclerosis. If the mice received special food to trigger atherosclerosis, the receptor was upregulated after only a month – which is to say, at a rather early stage of the disease. Mice that are unable to produce GPR55 developed larger atherosclerotic plaques compared to the wild type. In these mice, B cells were over-activated without GPR55 and inflammatory processes were promoted accordingly.When the researchers investigated human atherosclerotic plaques, they discovered that less receptor was present in unstable plaques with a high risk of triggering a stroke compared to stable plaques. “This finding indicates that the expression of the protein changes over the course of the disease,” reports Steffens.“Our results point to a protective role of the B cell GPR55 signaling pathway in atherosclerosis, which has potential relevance for human pathophysiology,” says Steffens. She hopes that “GPR55 can be the starting point for novel therapies.” Whether small molecules can be successfully deployed as active ingredients to stimulate the formation of GPR55 will be the work of further studies to establish.
