The IL2 gene encodes Interleukin-2, a crucial cytokine primarily secreted by activated CD4+ and CD8+ T lymphocytes, and to a lesser extent, by natural killer (NK) cells. This protein, also known as T-cell growth factor, plays a pivotal role in regulating immune responses by promoting the growth, proliferation, and differentiation of various "disease-fighting blood cells", including T cells, B cells, NK cells, monocytes, macrophages, and oligodendrocytes ^[1]. IL2 expression is tightly regulated; it is upregulated upon T-cell activation through T-cell receptor signaling and can be inhibited by factors like TOB and TGF-beta ^[2]. The encoded IL-2 protein mediates its effects by binding to the IL-2 receptor (IL-2R), a complex found on lymphocytes, which then activates downstream signaling pathways such as JAK-STAT, PI3K/Akt/mTOR, and MAPK/ERK, influencing T-cell survival, differentiation, and the maintenance of immune tolerance by supporting regulatory T cells (Tregs) while inhibiting pro-inflammatory Th17 cell differentiation ^[3]. Deregulation of IL2 function, whether due to deficiency or excess, is implicated in various autoimmune diseases, including systemic lupus erythematosus (SLE), rheumatoid arthritis (RA), systemic sclerosis, Sjögren's syndrome, and multiple sclerosis, as well as certain cancers like metastatic melanoma, renal cell carcinoma, and non-Hodgkin lymphoma ^[4].

The B6-hIL2 mouse is a humanized model, constructed by replacing the coding sequences of the endogenous mouse Il2 gene with the coding sequences of the human IL2 gene. B6-hIL2 mice can be used for research into the pathogenesis of autoimmune disorders like systemic lupus erythematosus (SLE), rheumatoid arthritis (RA), systemic sclerosis, Sjögren's syndrome, multiple sclerosis, and type 1 diabetes, as well as for the screening, development, and safety evaluation of IL2-targeted drugs.