Il7r, the gene encoding interleukin-7 receptor α chain (IL-7Rα), is a crucial component of the IL-7 receptor. IL-7R consists of IL-7Rα and γc chains, and is a member of the γc family of receptors for cytokines such as IL-2,-4,-9,-15, and-21. The IL-7/IL-7R signaling pathway functions through major signals via JAK1, JAK3 to STAT5, as well as non-canonical STAT3, STAT1, PI3K/AKT and MEK/ERK pathways. This pathway is essential for the development, homeostatic survival, and differentiation of lymphoid cells, including immature thymocytes, naïve T-cells, memory T-cells, pro-B-cells, and innate lymphocytes [2].

In disease research, in adult acute myeloid leukemia patients with t(8;21), low IL7R transcript level at diagnosis predicted relapse, potentially due to differences in T-cell quantity, status, and function [1]. In T-cell acute lymphoblastic leukemia, mutant IL7R alone can induce T-ALL with long-latency in transgenic zebrafish, and it collaborates with Myc to drive early-onset T-ALL, activating STAT5 and AKT pathways and enriching for leukemia-propagating cells [3]. In acute myeloid leukemia, 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 homeostasis through the IL-7/IL-7R signaling pathway. Research using genetic models like transgenic zebrafish and human patient-based genetic analysis has revealed its significant role in leukemia prognosis and pathogenesis. Understanding Il7r function provides insights into lymphoid-related biological processes and disease mechanisms, potentially guiding new therapeutic strategies for leukemia.