Il4ra, the interleukin-4 receptor alpha subunit, is crucial in immune-related processes. It is part of two receptor types that have different modulatory effects on immune responses. IL-4 and its receptor play important roles in the pathologies of asthma and atopy, with Il4ra being central to the signaling of IL-4 and IL-13, key drivers of type 2 inflammation [1,2].

In rhabdomyosarcoma (RMS), conditional deletion of Il4ra in genetically-engineered RMS mouse models altered the latency, site, and/or stage distribution of RMS tumors. In alveolar rhabdomyosarcoma (ARMS), satellite cell co-injection was necessary for Il4ra null tumor cells engraftment, while in embryonal rhabdomyosarcoma (ERMS), satellite cell co-injection decreased the latency of engraftment of Il4ra wild-type tumor cells but not Il4ra null tumor cells. This indicates that Il4ra is involved in the interaction between satellite cells and RMS tumor cells during tumor initiation [3].

In conclusion, Il4ra is essential for normal immune-related functions, especially in type 2 inflammation-associated processes. The study of Il4ra using gene-knockout mouse models in RMS has revealed its significance in tumor initiation and progression, providing insights into potential therapeutic targets for this disease.