Immunophenotyping

Clonality of CLL is confirmed by restricted light chain (kappa or lambda) expression on the cell surface,1,18 the presence of unique idiotypic specificities on the immunoglobulins produced by CLL cells,30 by immunoglobulin gene rearrangement analysis, and at times by detection of a specific cytogenetic abnormality.31 Using sensitive techniques, monoclonal proteins can be detected in the serum of many patients,32-34 although only 10 to 20 percent produce large enough quantities of monoclonal proteins to be detected by routine serum electrophoresis. The CLL cells express the B-cell markers CD19, CD20, CD21, and CD23; most CLL cells are also positive for Ia (DR and DC), Fc receptors, and have receptors for mouse erythrocytes.35-37 Some surface markers that are usually found on normal B cells, including CD22, are found infrequently on CLL cells. The hallmark of CLL is coex-pression of a common T-cell marker, CD5. Another disease entity in which B lymphocytes also express CD5 is mantle-cell lymphoma. Caution must be taken to differentiate CLL from the leukemic phase of mantle-cell lymphoma because the prognosis and treatment of these diseases are quite different. Use of antibody to the cell-surface antigen CD23 is most useful because this antigen is found on CLL lymphocytes but not on mantle cells. Rearrangements of immunoglobulin heavy- and light-chain genes are readily demonstrated in patients with CLL.38 In addition, almost 25 percent of patients with CLL have rearrangements of the T-cell receptor P gene.39,40

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