Abstract
Background and Aims : Upon atherosclerosis progression, mast cells accumulate within atherosclerotic plaques and activation of mast cells contributes to the progression and destabilization of plaques. Mast cells can be activated by crosslinking of the Fcε-receptor-I (FcεRI) with IgE-antigen complexes. Bruton’s tyrosine kinase (BTK) is involved in the downstream signaling of FcεRI-mediated mast cell activation and degranulation. In this study, we assessed the effects of the BTK inhibitor Acalabrutinib on FcεRI-mediated mast cell activation, plaque progression and destabilization in an atherosclerotic mouse model.
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