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Imbalance of T-cell subpopulations does not result in defective helper function in chronic lymphocytic leukemia
The T-lymphocyte subpopulations identified by the Fc receptors for IgG (TG cells) and IgM (TM cells) in 12 patients with B-cell chronic lymphocytic leukemia (CLL) were quantitated and studied for functional capabilities in an in vitro assay. The TG cells in patients were elevated in relation to age- and sex-matched normal controls (P less than 0.05) resulting in an altered TM/TG ratio of 1.8 +/- 0.76 in CLL versus 5.9 +/- 3.7 in controls (mean +/- SD, P less than 0.001). Despite this altered of B cells was found to be normal as reflected by the mean helper-suppressor score of 0.77 +/- 0.13 (+/- SEM) obtained for both patients and controls. This unimpaired capacity of the T cells from CLL patients to help normal B cells mature into immunoglobulin-secreting cells indicated that hypogammaglobulinemia and monoclonal serum immunoglobulins in these patients may be a result of either an intrinsic defect in the B lymphocytes or their replacement by a neoplastic clone rather than a defect in the immunoregulatory T cells.
The T-lymphocyte subpopulations identified by the Fc receptors for IgG (TG cells) and IgM (TM cells) in 12 patients with B-cell chronic lymphocytic leukemia (CLL) were quantitated and studied for functional capabilities in an in vitro assay. The TG cells in patients were elevated in relation to age- and sex-matched normal controls (P less than 0.05) resulting in an altered TM/TG ratio of 1.8 +/- 0.76 in CLL versus 5.9 +/- 3.7 in controls (mean +/- SD, P less than 0.001). Despite this altered of B cells was found to be normal as reflected by the mean helper-suppressor score of 0.77 +/- 0.13 (+/- SEM) obtained for both patients and controls. This unimpaired capacity of the T cells from CLL patients to help normal B cells mature into immunoglobulin-secreting cells indicated that hypogammaglobulinemia and monoclonal serum immunoglobulins in these patients may be a result of either an intrinsic defect in the B lymphocytes or their replacement by a neoplastic clone rather than a defect in the immunoregulatory T cells.