The main focus of the group is to decipher how the B cell receptor (BCR) signaling strength is controlled by T-cell dependent and T-cell independent stimuli, with a special emphasis on CD45 phosphatase activity. CD45 phosphatase is a key regulator of the BCR signaling pathway with the ability to enhance BCR signaling kinase activity. We have discovered that T-cell dependent- and independent-factors positively regulate BCR signaling via CD45 activity increase. By mapping mechanisms that regulate CD45 activity, and thus, BCR signaling strength, we identify targets that control B cell proliferation and differentiation into memory and plasma cells. We aim to pinpoint the natural ligands of CD45 and their functional modulation in order to identify novel therapeutic targets in B cell driven diseases of autoimmune and malignant origin.
Integration of T helper and BCR signals governs enhanced plasma cell differentiation of memory B cells by regulation of CD45 phosphatase activity
Cell Rep, 36 (6), 109525
Regular Exercise May Restore Certain Age-Related Alterations of Adaptive Immunity and Rebalance Immune Regulation
Front Immunol, 12, 639308
The Imbalance of Circulating Follicular T Helper Cell Subsets in Primary Sjögren's Syndrome Associates With Serological Alterations and Abnormal B-Cell Distribution
Front Immunol, 12, 639975