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Neuropathy and anti‐myelin‐associated glycoprotein IgM M proteins: T cell regulation of M protein secretion in vitro
Author(s) -
Latov Norman,
Godfrey Maurice,
Thomas Yoland,
NobileOrazio Eduardo,
Spatz Linda,
Abraham Judith,
Perman Gayle,
Freddo Lorenza,
Chess Leonard
Publication year - 1985
Publication title -
annals of neurology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.764
H-Index - 296
eISSN - 1531-8249
pISSN - 0364-5134
DOI - 10.1002/ana.410180204
Subject(s) - idiotype , secretion , pokeweed mitogen , microbiology and biotechnology , myelin associated glycoprotein , biology , cytotoxic t cell , monoclonal antibody , antibody , t cell , glycoprotein , in vitro , immunology , immune system , endocrinology , myelin , biochemistry , concanavalin a , central nervous system
Abstract 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 OKT 4 + T‐helper cells and the helper effect was inhibited by OKT 8 + 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.