Nivolumab-induced Myocarditis Successfully Treated with Corticosteroid Therapy: A Case Report and Review of the Literature

Matsuo, Keisuke; Ishiguro, Takashi; Najama, Takatomo; Shimizu, Yoshihiko; Kobayashi, Yasuhito; Mutou, Makoto

Nine of the 13 patients underwent a myocardial biopsy or autopsy (2, (4) (5) (6) (8) (9) (10) (11) (12) . All patients had myocardial tissue fibrosis, inflammatory cell infiltration, and T cell-dominant lymphocyte infiltration, findings that were also found in our patient. From previous reports, the characteristic histological finding of nivolumab-induced myocarditis is T-cell inflammation. Four potential mechanisms of ir-AE have been proposed (17) . First, ICIs (monoclonal antibodies) binding directly to cell surface proteins, such as cytotoxic T lymphocyte antigen 4 (CTLA4), which is expressed on normal tissues, can cause T-cell infiltration and injury to tissues due to complement mediation. Second, circulating T cells that rec-ognize antigens expressed by tumor cells can identify either the same tumor antigen or a homologous tissue antigen in healthy tissue. ICI therapy that inhibits programmed cell death protein 1 or CTLA4 can stimulate recognition of or binding of T cells to antigens expressed by non-target organs. Third, there is some evidence to suggest that inhibiting immune checkpoint molecules can increase circulating cytokine levels in affected tissues, thus helping inflammatory molecules infiltrate non-target tissues. Fourth, antibodies administered against ICIs may increase autoantibody levels against target organs or stimulate new autoantibody formation.