A number of target molecules are overexpressed on CLL cells, in some or all cases, including the interleukin-4 receptor (IL-4R), 1D10, CD5, CD18, CD19, CD20, CD21, CD22, CD23, CD24, CD25, CD27, CD29, CD38, CD43, CD44, CD45, CD47, CD50, CD52, CD54, CD55, CD59, CD62L, CD70, CD72, and CD102 (Table 1). A truncated form of CD79b that arises by alternative slicing of the CD79b gene with loss of exon 3 is commonly seen. CD22 is weakly expressed. The Na+/H+ antiporter, CD80, and CD86 are absent or poorly expressed. CD11a, CD49c, CD49d, and CD49e are variably expressed. The cell surface phenotype has been characterized by immuno-fluorescent staining with flow cytometry, immunohistochemistry, and immunoblots. Many of these cell surface markers are useful in diagnosis and in explaining some of the clinical findings of patients with CLL.
The coexpression of C5 and CD19 has been used to confirm the diagnosis of CLL (7). Expression of CD23 and CD25 helps to differentiate CLL from mantle cell lymphoma (8). The level of expression of CD38 has been used to predict the clinical course (9). CD55 and CD59 expression may correlate with patient responsiveness to rituximab (see Subheading 4. below) (10). The coexpression of CD27 and CD70 may modify accessory cell function and reduce the ability to activate T cells (11). The CD49d-CD29 complex (a403) integrin binds to vascular cell adhesion molecule-1 (VCAM-1) on stimulated endothelium in the bone marrow and secondary lymphoid organs (12). This will lead to accumulation of CLL cells at these sites. Integrin binding also has an anti-apoptotic function. The truncated CD79b disrupts normal B-cell receptor structure and function (13).
A number of these surface antigens are poorly expressed on nonhematopoietic tissues and have been developed as targets for monoclonal antibodies or cytokines.
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