Interleukin-7 (IL7) is a cytokine belonging to the family of cytokines with four anti-parallel α helixes that bind Type I cytokine receptors [2]. It plays a non-redundant role in T cell survival and homeostasis, and is also required for the development and homeostatic survival of lymphoid cells [1,2]. The major signals of IL7 receptor transduction are through JAK1, JAK3 to STAT5 and via non-canonical STAT3, STAT1, PI3K/AKT and MEK/ERK pathways [2].

IL7-deficient mice exhibit severe T cell lymphopenia, demonstrating the crucial role of IL7 in T cell maintenance [1]. In humans, deficiencies in the IL7 pathway lead to severe combined immunodeficiency due to lymphopenia [2]. Excessive IL7 pathway signaling in mice drives autoimmune diseases, and in humans, it is associated with autoimmune syndromes such as multiple sclerosis, type 1 diabetes, rheumatoid arthritis, sarcoidosis, atopic dermatitis, and asthma [2]. Mutations in the IL7 receptor pathway can drive acute lymphoblastic leukemia [2].

In conclusion, IL7 is essential for the survival of various lymphoid cells, especially T cells, and its dysregulation is associated with multiple diseases, including immunodeficiencies, autoimmune diseases, and leukemia. The study of IL7-deficient mouse models has significantly contributed to understanding its role in these disease conditions.