Il5ra, also known as Interleukin 5 receptor, alpha, is a well-established regulator of eosinophil activation. It is involved in eosinophil-mediated anti-parasitic activities and allergic reactions [2]. It has been implicated in pathways such as the PI3K-Akt signaling pathway and Natural killer cell mediated cytotoxicity [1].

In multiple myeloma, IL5RA was upregulated and associated with disease progression. In vitro and in vivo experiments showed its involvement in apoptosis, proliferation, and drug resistance of myeloma cells, suggesting it could be an immunogenic cell death-related predictor [1].

In pulmonary fibrosis, epithelial IL5RA was upregulated during disease progression and promoted epithelial-mesenchymal transition (EMT) via the Jak2/STAT3 cascade. Inhibiting IL5RA might offer a therapeutic strategy [2].

In chronic obstructive pulmonary disease (COPD), IL5RA gene variants were significantly associated with susceptibility to the disease. Rs13097407 reduced susceptibility, while rs3856850 increased the risk, and the effects were influenced by sex and smoking [3].

In conclusion, Il5ra plays essential roles in regulating eosinophil activation and is involved in multiple biological processes and diseases. Studies on Il5ra, especially through in vitro and in vivo models, have provided insights into its role in diseases like multiple myeloma, pulmonary fibrosis, and COPD, which may contribute to the development of new therapeutic strategies.