Further studies showed that tumor-derived IgG directly interacted with sialic acid-binding Ig-type lectins (Siglecs), including Siglec-7 and Siglec-10, on effector CD4+ and CD8+ T cells by its sialylation of the CH1 domain, which finally led to the immunosuppressive effect of T cells and the promotion of tumor growth. Here, CD4 is linked to neoplasm.