Journal article

Alarmin-activated B cells accelerate murine atherosclerosis after myocardial infarction via plasma cell-immunoglobulin-dependent mechanisms

Tin Kyaw, Paula Loveland, Peter Kanellakis, Anh Cao, Axel Kallies, Alex L Huang, Karlheinz Peter, Ban-Hock Toh, Alex Bobik

EUROPEAN HEART JOURNAL | OXFORD UNIV PRESS | Published : 2021

Abstract

AIMS: Myocardial infarction (MI) accelerates atherosclerosis and greatly increases the risk of recurrent cardiovascular events for many years, in particular, strokes and MIs. Because B cell-derived autoantibodies produced in response to MI also persist for years, we investigated the role of B cells in adaptive immune responses to MI. METHODS AND RESULTS: We used an apolipoprotein-E-deficient (ApoE-/-) mouse model of MI-accelerated atherosclerosis to assess the importance of B cells. One week after inducing MI in atherosclerotic mice, we depleted B cells using an anti-CD20 antibody. This treatment prevented subsequent immunoglobulin G accumulation in plaques and MI-induced accelerated atheros..

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Grants

Awarded by National Health and Medical Research Council of Australia


Awarded by Contributing to Australian Scholarship and Science (CASS) Foundation


Funding Acknowledgements

This work was supported by grants from the National Health and Medical Research Council of Australia (Investigator grant to K.P., Project grant 1002333 to B.-H.T. and A.B.) and the Contributing to Australian Scholarship and Science (CASS) Foundation (SM/13/4956 to T.K.) and in part by the Victorian State Government Operational Infrastructure Support grant.