Passive transfer of PBMCs and IgG from a patient with COVID-19 myocarditis into mice induced higher cardiac IFN-γ expression compared with healthy control components.
Case Report (n=1)
The study demonstrates that cellular reactivity to SARS-CoV-2 spike protein and myocardial tissue, along with increased IFN-γ production, suggests an autoimmune mechanism in COVID-19-associated myocarditis.
Myocarditis has been described following SARS-CoV-2 infection. The mechanisms underlying COVID-19-associated myocarditis remain incompletely understood. Peripheral blood mononuclear cells (PBMCs), IgG fractions, and myocardial biopsy tissue were obtained from a patient with COVID-19 myocarditis. Cellular responses to SARS-CoV-2 spike protein and myocardial tissue extract were assessed in vitro. PBMCs and purified IgG were passively transferred into Rag2/IL2RG-/- mice. Interferon-gamma (IFN-γ) production and cardiac IFN-γ transcript levels were measured. PBMCs from the myocarditis patient proliferated in response to spike protein and myocardial tissue extract, whereas PBMCs from a healthy control did not. PBMCs from the patient secreted higher concentrations of IFN-γ compared with the healthy control. Introduction of patient PBMCs or IgG into Rag2/IL2RG-/- mice resulted in higher cardiac IFN-γ transcript levels compared with control PBMCs or IgG. These findings demonstrate cellular reactivity to SARS-CoV-2 spike protein and myocardial tissue, increased IFN-γ production, and induction of cardiac IFN-γ expression following passive transfer of immune components.
Tuvali et al. (Mon,) conducted a case report in COVID-19 myocarditis (n=1). Passive transfer of patient PBMCs and IgG vs. Healthy control PBMCs and IgG was evaluated on Cellular proliferation, IFN-γ production, and cardiac IFN-γ transcript levels. Passive transfer of PBMCs and IgG from a patient with COVID-19 myocarditis into mice induced higher cardiac IFN-γ expression compared with healthy control components.