In patients with plasma cell dyscrasia, individual clones of antibody-producing cells proliferate abnormally and secrete monoclonal antibodies or M proteins in excess. The cause of the monoclonal proliferation of lymphocytes and M protein secretion is unknown and it is not known whether the M protein-secreting B cells are autonomous or capable of responding to regulatory T cells. We carried out experiments using lymphocytes from a patient with neuropathy and plasma cell dyscrasia whose IgM M protein bound to the myelin-associated glycoprotein (MAG) to determine whether secretion of the M protein in vitro was responsive to T cell help or suppression. M protein secretion was measured by an enzyme-linked immunosorbent assay system for measuring anti-MAG IgM, and the number of M protein-secreting lymphocytes was enumerated by a reverse hemolytic plaque assay specific for the M protein idiotype. The patient's B cells were maximally stimulated by pokeweed mitogen-activated autologous OKT4+ T-helper cells and the helper effect was inhibited by OKT8+ suppressor/cytotoxic T cells. Low levels of M protein secretion in the absence of T cells were also observed and there was partial stimulation of M protein secretion by T cells in the absence of pokeweed mitogen.
|Titolo:||Neuropathy and anti-myelin-associated glycoprotein IgM M proteins: T cell regulation of M protein secretion in vitro|
|Parole Chiave:||Blood Proteins; Myelin Proteins; Humans; Cell Separation; B-Lymphocytes; Lymphocyte Cooperation; Waldenstrom Macroglobulinemia; Myelin-Associated Glycoprotein; Autoantibodies; Peripheral Nervous System Diseases; Immunoglobulin M; Immunoglobulins; T-Lymphocytes|
|Settore Scientifico Disciplinare:||Settore MED/26 - Neurologia|
|Data di pubblicazione:||ago-1985|
|Digital Object Identifier (DOI):||10.1002/ana.410180204|
|Appare nelle tipologie:||01 - Articolo su periodico|