Il17ra, the gene encoding interleukin-17 receptor A, is a common receptor for IL-17A and IL-17F. It is involved in the IL-23/IL-17 immune axis, which plays a crucial role in T cell lineage commitment and function, and is associated with immune-mediated inflammatory diseases [3].

In pancreatic cancer, deletion of Il17ra from the pancreatic epithelial compartment, but not the hematopoietic compartment, led to delayed initiation and progression of premalignant lesions and increased infiltration of CD8+ cytotoxic T cells, indicating that pancreatic epithelial Il17ra promotes pancreatic tumorigenesis by reprogramming the immune pancreatic landscape [1].

In Fanconi anemia, polymorphisms in the Il17ra gene (rs917864 [T allele] and rs17606615 [T allele]) were associated with age and the presence of leukoplakia, suggesting its role in this rare autosomal recessive disease [2].

In ulcerative colitis, gingerenone A was shown to protect against the disease by directly interacting with Il17ra protein to inhibit inflammatory signaling activation [4].

In pancreatic ductal adenocarcinoma (PDAC), Il17ra expressed by fibroblasts was required for Tc17-driven tumour growth, as Tc17-CM induced inflammatory CAF differentiation in an Il17ra-dependent manner [5].

In conclusion, Il17ra is essential in multiple disease processes. Gene knockout or polymorphism studies in relevant mouse models have revealed its role in pancreatic cancer, Fanconi anemia, ulcerative colitis, and PDAC. These findings contribute to understanding the disease mechanisms and potentially developing new therapeutic strategies.