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. 2023 Feb 23;14:1130438. doi: 10.3389/fimmu.2023.1130438

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Copyright © 2023 Li, Peng, Wu, Yeung and Yang

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Possible mechanisms of CV-irAE. (A) Activated T cells not only attack tumor cells but also cross-reactivate with cardiac muscle. (B) Cardiac myocytes secrete cTnI antibodies after using ICIs. (C) Myosin-specific T cells TCRs can recognize myosin and drive cytotoxic T-cell-mediated killing. (D) ICIs can lead to increased levels of pro-inflammatory cytokines. (E) Systemic application of ICI may disrupt immune homeostasis between cytotoxic T cells and Tregs. (F) ICIs may contribute to plaques progression and coronary events. (G) Anti-PD-L1 monoclonal antibodies may mediate NK cells killing cardiomyocytes through the ADCC pathway.