Table 1:

Predictors of adverse events following checkpoint inhibitor therapy

Genotype	• High risk T1D HLA alleles, such as HLA-DR4, in patients with CPI-induced DM [10, 14] • HLA-DRB1*04:05 association with CPI-induced inflammatory arthritis [33] • HLA-DRB1*11:01 association with CPI-induced pruritis [48]
History of autoimmune disease	• irAEs may be more frequent and occur sooner in patients with underlying autoimmune disease [49, 50]
Baseline autoantibodies	• Presence of thyroid autoantibodies at baseline increase risk of thyroid dysfunction [28–30] • Skin irAEs may be more frequent in patients with positive RF at baseline [30] • Baseline autoantibody signatures, such as those targeting TNFα signaling pathways may be predictive of irAEs [34]
Cytokine levels	• Baseline IL-17 levels may predict CPI-induced colitis [38] • IL-1β, IL-2, and GM-CSF at baseline and early decreases in IL-8, G-CSF, and MCP-1 predict thyroid dysfunction [41] • Cytokine toxicity score predictive of severe irAEs [93]
Immune cell changes	• Reduction in circulating B cells, increase in CD21lo PD-1+ B cells and plasmablasts precede adverse events [25] • Neutrophil-to-lymphocyte ratio and platelet-to-lymphocyte ratio may predict appearance of irAEs [94]
Microbiome	• Baseline microbiome enriched for Faecalibacterium predictive of colitis [43] • Abundance of Bacteroidetes phylum may be protective for development of colitis [44]
Tumor burden	• High tumor burden in NSCLC associated with higher risk of severe irAEs [95]

Abbreviations: DM: diabetes, G-CSF: granulocyte colony-stimulating factor, GM-CSF: granulocyte-macrophage colony-stimulating factor, HLA: human leukocyte antigen, irAE: immune-related adverse event, MCP-1: monocyte chemoattractant protein-1, NSCLC: non-small cell lung cancer, RF: rheumatoid factor, T1D: type 1 diabetes