Secretions of anti-myelin-associated glycoprotein antibodies by B cells from patients with neuropathy and nonmalignant monoclonal gammopathy.
Four patients with peripheral neuropathy and nonmalignant monoclonal gammopathy with anti-myelin-associated glycoprotein (MAG) antibodies were studied to determine whether secretion of anti-MAG IgM antibodies by B cells was autonomous, or whether the monoclonal B cells were responsive to T cells. Secretion of anti-MAG IgM by isolated B cells was stimulated by the addition of increasing numbers of pokeweed mitogen (PWM)-activated autologous OKT4+ helper T cells in all four patients. Secretion of anti-MAG IgM by peripheral blood lymphocytes was dependent on the ratio of OKT4+ T helper cells to OKT8+ T suppressor/cytotoxic cells. In three patients with an OKT4+ to OKT8+ T-cell ratio of 2:1, PWM activation stimulated secretion of anti-MAG IgM; in one patient with an OKT4+ to OKT8+ ratio of 1:2, activation by PWM suppressed anti-MAG IgM secretion. These studies suggest that the monoclonal B cells that secrete anti-MAG IgM are responsive to regulatory T cells.
D001402:B-Lymphocytes / Q000276:immunology*; D001798:Blood Proteins / Q000032:analysis*; D006801:Humans; D006942:Hypergammaglobulinemia / Q000276:immunology*; D007074:Immunoglobulin G / Q000032:analysis; D007075:Immunoglobulin M / Q000032:analysis*; D007136:Immunoglobulins / Q000235:genetics; D008998:Monoclonal Gammopathy of Undetermined Significance / Q000276:immunology*; D009185:Myelin Proteins / Q000276:immunology*; D018992:Myelin-Associated Glycoprotein; D010523:Peripheral Nervous System Diseases / Q000276:immunology*; D013601:T-Lymphocytes / Q000502:physiology
D001798:Blood Proteins; D007074:Immunoglobulin G; D007075:Immunoglobulin M; D007136:Immunoglobulins; C009823:M-proteins (Myeloma); D009185:Myelin Proteins; D018992:Myelin-Associated Glycoprotein