B-lymphocyte antigen CD19 (CD19) and B-lymphocyte antigen CD22 (CD22) (CD19/CD22)

B-lymphocyte antigen CD19 (CD19) and B-lymphocyte antigen CD22 (CD22) are surface glycoproteins predominantly expressed on B-lineage cells and are key therapeutic targets in B-cell malignancies [4, 7]. CD19 is a member of the immunoglobulin superfamily that functions as a critical co-receptor for the B-cell receptor (BCR), significantly enhancing signaling and lowering the threshold for B-cell activation [4]. CD22 is a sialic acid-binding Ig-like lectin (Siglec-2) that typically acts as an inhibitory co-receptor to modulate BCR signaling and maintain B-cell homeostasis [4, 7]. In clinical oncology, dual targeting of CD19 and CD22—most notably through bispecific chimeric antigen receptor (CAR) T-cell therapy—is employed to address the challenge of "antigen escape," where tumor cells lose CD19 expression to evade monospecific treatments [1, 5]. By simultaneously targeting both antigens, these therapies aim to achieve more comprehensive tumor eradication and reduce the incidence of relapse in patients with refractory B-cell acute lymphoblastic leukemia (B-ALL) or non-Hodgkin lymphoma (NHL) [2, 3, 8]. Notable safety concerns include cytokine release syndrome (CRS) and neurotoxicity, which are common to potent T-cell engaging therapies [11, 12].

Other names

CD19CD22B-cell surface antigen B4Siglec-2BL-CAMLeu-12CD19xCD22CD19/CD22 dual target

Dual-antigen targeting via chimeric antigen receptor (CAR) T-cells or bispecific antibodies to induce B-cell lysis and prevent antigen escape [1, 5]. The mechanism involves the simultaneous or sequential engagement of CD19 and CD22 surface antigens, leading to the formation of an immunological synapse and subsequent cytotoxic destruction of malignant B-cells [2, 4, 15].