Il7r, encoding the interleukin-7 receptor α chain, is a crucial component in the interleukin-7 (IL-7) signaling pathway. IL-7R is a member of the γc family of receptors for cytokines IL-2,-4,-9,-15, and-21. Signals from IL-7R mainly transduce through JAK1, JAK3 to STAT5 and also via non-canonical STAT3, STAT1, PI3K/AKT and MEK/ERK pathways. It is essential for the development, homeostatic survival and function of lymphoid cells, including T-cells, B-cells and innate lymphocytes [2].

In acute myeloid leukemia (AML) patients with t(8;21), low IL7R expression at diagnosis predicted relapse, likely due to differences in T-cell quantity, status and function [1]. Mutant IL7R can collaborate with MYC to induce T-cell acute lymphoblastic leukemia (T-ALL) in transgenic zebrafish models, highlighting its role in leukemogenesis [3]. In addition, in AML, IL7R mutations are associated with an inferior prognosis, including higher non-relapse mortality, shorter overall survival and event-free survival, even in patients who have undergone hematopoietic stem cell transplantation [4].

In conclusion, Il7r is vital for lymphoid cell development and function. Studies using genetic models such as transgenic zebrafish and analysis of patient samples with IL7R mutations have revealed its significant role in leukemia, both in terms of prognosis and leukemogenesis. Understanding Il7r function provides insights into disease mechanisms and potential therapeutic targets for leukemia.