Interleukin-7 (IL7) is a cytokine belonging to the family of cytokines with four anti-parallel α helixes that bind Type I cytokine receptors. 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 producers of IL7 are stromal cells in thymus, bone marrow and lymphoid organs. Its production is primarily constitutive but can be affected by IFNγ and other factors. IL7 signals mainly through JAK1, JAK3 to STAT5 and also via non-canonical STAT3, STAT1, PI3K/AKT and MEK/ERK pathways [2].

IL7-deficient mice exhibit severe T cell lymphopenia, demonstrating its crucial role in T cell survival [1]. Deficiencies in the IL-7 pathway in both humans and mice lead to severe combined immunodeficiency due to lymphopenia [2]. Excessive signaling of the IL7 pathway 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. Mutations in the IL-7 receptor pathway can drive acute lymphoblastic leukemia [2].

In conclusion, IL7 is essential for the survival of various lymphoid cells, especially T cells. Studies on IL7-deficient mouse models have revealed its key role in maintaining immune system homeostasis and its implications in immunodeficiency, autoimmune diseases and leukemia. Understanding IL7's function can potentially lead to new strategies for treating these related diseases.

References:

1. Park, Jung-Hyun, Waickman, Adam T, Reynolds, Joseph, Castro, Mario, Molina-París, Carmen. 2019. IL7 receptor signaling in T cells: A mathematical modeling perspective. In Wiley interdisciplinary reviews. Systems biology and medicine, 11, e1447. doi:10.1002/wsbm.1447. https://pubmed.ncbi.nlm.nih.gov/31137085/

2. Winer, Hila, Rodrigues, Gisele O L, Hixon, Julie A, Li, Wenqing, Durum, Scott K. 2022. IL-7: Comprehensive review. In Cytokine, 160, 156049. doi:10.1016/j.cyto.2022.156049. https://pubmed.ncbi.nlm.nih.gov/36201890/