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The following is a summary of “Monocytic reactive oxygen species-induced T cell apoptosis impairs cellular immune response to SARS-CoV-2 mRNA vaccine,” published in the January 2025 issue of Allergy and Immunology by Gimenez et al. 

During acute severe COVID-19, the SARS-CoV-2 spike protein (S) induces T cell apoptosis by increasing Angiotensin II (AngII) levels. This triggers monocytic reactive oxygen species (ROS) release and programmed T cell death through ACE2 receptor protease activity. 

Researchers conducted a retrospective study to test if SARS-CoV-2 mRNA vaccines trigger the same cascade as the virus, inducing T cell apoptosis via monocytic ROS release from the S-protein receptor binding domain (RBD). 

They used ELISA to quantify RBD and AngII levels in peripheral blood mononuclear cells (PBMCs) and interferon-γ in supernatants exposed to S. Monocytic ROS production, T cell apoptosis, and S-induced T lymphocyte proliferation were measured by flow cytometry. DNA damage was assessed using immunofluorescence. 

The results showed circulating RBD peaked on day 14, correlating with an increase in AngII levels peaking on Day 28. This increase was linked to monocyte ROS production, ROS-mediated DNA damage in PBMCs, CD4⁺ and CD8⁺ T lymphocyte apoptosis, and a poor response to S in vitro from both T cell types. 

Investigators observed that the vaccinal antigen triggered the same cascade as SARS-CoV-2 infection, which may explain the suboptimal vaccine efficiency, limited memory, and side effects. AngII receptor antagonists and antioxidants were suggested to improve vaccine performance. 

Source: jacionline.org/article/S0091-6749(25)00011-9/abstract