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. Author manuscript; available in PMC: 2022 Feb 18.
Published in final edited form as: J Cardiovasc Transl Res. 2020 Apr 6;13(3):402–416. doi: 10.1007/s12265-020-09992-5

Fig. 1.

Fig. 1

Proposed Mechanisms of Cardiotoxicity from Immune Checkpoint Inhibitors. Top: Tumor cell antigen interaction with TCR. A specific antigen present of the cell surface is recognized by the TCR of the T-cell, co-stimulation is inhibited by immune checkpoint therapy resulting in further T-cell effect. Bottom: Purposed cardiac autoimmunity by one of three mechanisms. 1) “Same antigen” the effector T-cell recognizes the same antigen on both the tumor and self-cardiac myocyte. 2) “Similar antigen” the antigen recognized by the effector T-cell is similar to the antigen recognized but not identical. This similarity is close enough to facilitate T-cell immunity against cardiac myocytes. 3) T-cell chimera where a single T cell has two different TCRs recognizing two different antigens (1 from the tumor, and 1 from the cardiac myocyte) both are recognized leading an effector T-cell response to both tumor and cardiac myocyte. TCR= T-cell receptor.