Il23r, the interleukin-23 receptor, is a key component in the interleukin-23 signaling pathway. IL-23, a heterodimeric cytokine, binds to Il23r, initiating a signaling cascade that involves the STAT3 pathway. This pathway is crucial in regulating the activation and differentiation of lymphocytes, playing an important role in maintaining immune homeostasis [4].

Genetic variants in Il23r have been associated with multiple diseases. In Crohn's disease, the rs11209026 variant in Il23r was associated with significant protection and a recessive mode of inheritance, suggesting its role in disease susceptibility [2]. Engineered Tregs expressing IL23R-CAR showed promise for treating active Crohn's disease, as IL23R-CAR Tregs could migrate to IL23R-expressing tissue and specifically activate against colon biopsy-derived cells from active CD patients [1]. In psoriasis, genetic variants within Il23r increase the disease risk, and the mutant (R381Q) protective form of Il23r led to differential expression of genes implicated in the disease, such as HLA-B, SOCS1, and RUNX3 [3]. Additionally, Il23r polymorphisms are associated with alopecia areata, and in Crohn's disease, expansion of apoptosis-resistant intestinal TNFR2 + IL23R + T cells is associated with resistance to anti-TNF therapy [5,6].

In conclusion, Il23r is essential for IL-23 signaling, which is crucial for immune regulation. Studies on genetic variants and engineered cell therapies related to Il23r have provided insights into its role in diseases like Crohn's disease, psoriasis, and alopecia areata. These findings may contribute to the development of new therapeutic strategies for these immune-related diseases.