CD19, a 95-kDa member of the immunoglobulin super-family, is exclusively expressed on B lymphocytes. It serves as a critical co-receptor for B cell antigen receptor (BCR) signal transduction. Co-ligation of CD19 with the BCR can synergistically enhance calcium release, mitogen-activated protein kinase activity, and cell proliferation. However, in some cases, CD19-deficient animals show hyper-responsiveness, indicating potential negative regulatory functions in BCR signaling. Abnormal CD19 expression can lead to B-cell related diseases [4].

CD19 is a B-lineage-specific transmembrane glycoprotein, expressed on over 95% of B-cell malignancies, making it an ideal target for immune therapies. Anti-CD19 chimeric antigen receptor (CAR) T cell therapies have shown promise in treating B-cell lymphoma and leukemia. For example, the CD19-BBz(86) CAR T cells in a phase 1 trial showed potent antilymphoma response without causing neurotoxicity or severe cytokine-release syndrome (CRS) [1]. In a murine model, anti-CD19-CAR-transduced T cells could eradicate lymphoma and normal B cells [3]. Additionally, CD19-targeted therapies like CAR T cells and Uplizna® (inebilizumab) are being explored for treating autoimmune diseases such as systemic sclerosis [2].

In conclusion, CD19 is crucial for B-cell function, with its abnormal expression linked to B-cell malignancies and autoimmune diseases. Studies using models like murine models with anti-CD19-CAR-transduced T cells have revealed its potential as a therapeutic target in treating B-cell-related diseases, highlighting the importance of understanding its functions for developing effective treatments [1,2,3,4].