Neuropathy and anti‐myelin‐associated glycoprotein IgM M proteins: T cell regulation of M protein secretion in vitro

Norman Latov, Maurice Godfrey, Yoland Thomas, Eduardo Nobile‐Orazio, Linda Spatz, Judith Abraham, Gayle Perman, Lorenza Freddo, Leonard Chess

Research output: Contribution to journalArticlepeer-review

23 Scopus citations

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 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.

Original languageEnglish (US)
Pages (from-to)182-188
Number of pages7
JournalAnnals of Neurology
Volume18
Issue number2
DOIs
StatePublished - Aug 1985

ASJC Scopus subject areas

  • Neurology
  • Clinical Neurology

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