huCD7 Mouse

The CD7 gene encodes a transmembrane glycoprotein belonging to the immunoglobulin superfamily (IgSF). As an important co-receptor on the T cell surface, CD7 plays a critical regulatory role in T cell activation, proliferation, and signal transduction. CD7 is primarily expressed on T cells and natural killer (NK) cells, with expression observed from the early stages of thymocyte development through to mature T cells. It is also expressed in some hematopoietic progenitor cells, but its expression level is relatively low in most normal non-T/NK cell tissues ^[1]. Aberrant expression or dysregulated signaling of CD7 is closely associated with various diseases. As a key therapeutic target in immunotherapy, CD7 is highly expressed in T cell acute lymphoblastic leukemia (T-ALL) and T cell lymphomas, making it a critical molecule for targeting T cell malignancies ^[1]. In addition, CD7 is associated with systemic sclerosis (SSc) and graft-versus-host disease (GvHD) ^[2-3]. Currently, multiple therapeutic strategies targeting CD7 are under development, including anti-CD7 CAR-T cell therapy, CD7 CAR-iNK cells, and bispecific CAR-T therapies targeting CD7, which have demonstrated promising preclinical and early clinical potential in relapsed/refractory T-ALL and T cell lymphomas ^[4-5].

The huCD7 mouse is a humanized model generated using gene editing technology, in which the endogenous signal peptide and extracellular domain sequence of the mouse Cd7 gene were replaced with the corresponding sequence of the human CD7 gene. This model is suitable for the in vivo efficacy and safety evaluation of antibody drugs and CAR-T cell therapies targeting human CD7, as well as for studies on T cell development and function. It also serves as an ideal platform for investigating the functional mechanisms of CD7⁺ T cells in T cell acute lymphoblastic leukemia (T-ALL), T cell lymphomas, and autoimmune diseases such as systemic sclerosis (SSc).