Cytokine release syndrome induced by anti-programmed death-1 treatment in a psoriasis patient: A dark side of immune checkpoint inhibitors

In recent years, cancer immunotherapy has introduced novel treatments, such as monoclonal antibodies, which have facilitated targeted therapies against tumor cells. Programmed death-1 (PD-1) is an immune checkpoint expressed in T cells that regulates the immune system's activity to prevent over-activation and tissue damage caused by inflammation. However, PD-1 is also expressed in tumor cells and functions as an immune evasion mechanism, making it a therapeutic target to enhance the immune response and eliminate tumor cells. Consequently, immune checkpoint inhibitors (ICIs) have emerged as an option for certain tumor types. Nevertheless, blocking immune checkpoints can lead to immune-related adverse events (irAEs), such as psoriasis and cytokine release syndrome (CRS), as exemplified in the clinical case presented by Zhou et al involving a patient with advanced gastric cancer who received sintilimab, a monoclonal antibody targeting PD-1. Subsequently, the patient experienced exacerbation of psoriasis and CRS. The objective of this editorial article is to elucidate potential immunologic mechanisms that may contribute to the development of CRS and psoriasis in patients receiving ICIs. It is crucial to acknowledge that while ICIs offer superior safety and efficacy compared to conventional therapies, they can also manifest irAEs affecting the skin, gastrointestinal tract, or respiratory system. In severe cases, these irAEs can lead to life-threatening complications such as circulatory shock or multiorgan failure. Consequently, it is recommended that patients receiving ICIs undergo regular monitoring to identify and manage these adverse events effectively.