Additionally, transcriptomic signatures of T cell activation and differentiation (CD28, ICOS, TCF7) were downregulated in the LC compared with the CC group at day 90–180 after infection (Fig. 2b), while CD8+ T cell exhaustion signatures and programmed cell death protein 1 (PDCD1) signaling-associated genes (IFI44, PRDM1, NR4A3, NFKBIA, MAFF) were significantly increased in the LC group (Fig. 2c), suggesting a potential role of T cell dysregulation in the pathogenesis of LC. Here, PRDM1 is linked to laryngotracheoesophageal cleft.