Immunoregulatory T-cell dysfunction in polyclonal gammopathy.

The mechanisms responsible for the increased serum immunoglobulines in polyclonal gammopathy states are unknown. We have studied the regulation of peripheral blood B-cell immunoglobulin synthesis and secretion, by T cells of either blood or bone marrow compartments, in 20 patients with polyclonal gammopathy and 27 controls with normal serum immunoglobulin levels. When compared to B-T-cell cocultures of normals, cocultures of polyclonal gammopathy patients had significantly higher levels of immunoglobulin secretion (P less than 0.01). Normal T cells but not T cells from patients with polyclonal gammopathy suppressed B-cell immunoglobulin secretion (P less than 0.01) and not the number of cytoplasmic immunoglobulin-positive cells of the polyclonal gammopathy patients. T cells from patients with polyclonal gammopathy enhanced normal B-cell immunoglobulin secretion (P less than 0.05) but not the number of cytoplasmic immunoglobulin-positive cells. Controls' bone marrow T cells were more efficient than blood T cells in suppressing polyclonal gammopathy B cells (P less than 0.02). T cells in polyclonal gammopathy are predominantly helper cells and could play a role in the enhanced immunoglobulin secretion of B cells. Bone marrow T cells are more efficient than blood T cells in regulating B cells. It seems that T cells predominantly regulate B-cell immunoglobulin secretion and not the number of B cells with cytoplasmic Ig.