Journal
PHARMACOLOGY
Volume 106, Issue 3-4, Pages 123-136Publisher
KARGER
DOI: 10.1159/000509081
Keywords
Cytotoxic T-lymphocyte-associated antigen 4; Programmed cell death protein-1; T cell; B cell; Antibody; Autoimmune; Cytokine; Cross-presentation
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ICIs have revolutionized cancer patient prognosis, but also carry the risk of severe inflammatory complications. Recent studies have advanced our understanding of irAEs development, focusing on potential pathways to prevent severe immune-related complications in patients undergoing cancer immunotherapy.
Immune checkpoint inhibitors (ICIs) have changed the prognosis of many cancer patients. Blocking antibodies targeting inhibitory cytotoxic T-lymphocyte-associated antigen 4 or programmed cell death protein-1 receptors or the programmed cell death ligand-1 have led to long-lasting remissions in patients with even advanced cancers. Main side effects induced by ICIs are inflammatory complications with sometimes severe sequelae for patients. Recent studies have improved our understanding how such immune-related adverse events (irAEs) develop. Here, we summarize the current knowledge of pathomechanisms involved in the de-velopment of irAEs with a particular focus on potential pathways that could be targeted to prevent severe immune-related complications in patients treated with cancer immunotherapy.
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