B‐lymphocyte suppression in multiple myeloma is a reversible phenomenon specific to normal B‐cell progenitors and plasma cell precursors

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Abstract
The reduced levels of normal immunoglobulin in patients with myeloma may be due to suppression of normal B‐cell differentiation. However, reports on the numbers of B cells vary, with some finding decreases consistent with immunoparesis, and others reporting expansions of phenotypically aberrant cells. We have therefore assessed the phenotype and levels of B lymphocytes in patients at presentation (n = 23), in plateau or complete remission (PB n = 42, BM n = 18), and in relapse (PB n = 17, BM n = 14), in comparison to normal individuals (n = 10). Phenotypic analysis was performed using five‐parameter flow cytometry, with CD14 used to exclude monocytes where necessary.We found no evidence of a phenotypically distinctive blood or marrow B‐cell population in patients with myeloma, nor of an increase in the levels of any B‐cell subset. Numbers of blood CD19+38+ normal plasma cell precursors were significantly reduced in presentation/relapse patients, but not in patients in plateau/remission. Total CD19+ cells were significantly reduced only in patients with circulating myeloma cells, detected by IgH‐PCR. In the marrow, CD19+ B cells expressing CD5, CD10, CD34, CD38, CD45low and Syndecan‐1 were significantly decreased at presentation/relapse, but not in patients in plateau/remission. The majority of these antigens are expressed by normal B‐cell progenitors, indicating that myeloma also affects the early stages of B‐cell development. The suppression of progenitor cells was not restricted to B‐lymphoid differentiation, as total CD34+ cells were also significantly reduced in the marrow of myeloma patients at presentation.These results indicate that, if neoplastic B cells are present in myeloma, they are low in number and have a phenotype similar to their normal counterparts. Furthermore, there is a reversible suppression of CD19+ B lymphocytes that correlates inversely with disease stage, and specifically affects the early and late stages of normal B‐cell differentiation.

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