Metabolic inhibition of plaque-forming cells: comparison of human rheumatoid-factor-producing cells with mouse anti-sheep erythrocyte-producing cells.
While rheumatoid-factor-producing haemolytic plaque-forming cells (RF--PFC) of the human peripheral blood were easily inhibited by cycloheximide, mouse spleen cells immune to sheep red cells (anti-SRC PFC) were inhibited only after prolonged preincubation in the drug. The RF--PFC were easily inhibited by propranolol, while the anti-SRC PFC were not at all inhibited. Vinblastine inhibited both systems equally. These differences are taken to suggest that the RF--PFC have very little preformed antibody in them and therefore depend upon active protein synthesis for their demonstration. In contrast, anti-SRC PFC, which may be predominantly mature plasma cells, generally need no new protein synthesis for their demonstration because of increased quantities of preformed antibody. A possible mechanism is that RF--PFC may represent primarily RF-specific B cells, the RF of which is released by surface immunoglobulin shedding and therefore susceptible to membrane stabilising agents such as propranolol.
D000818:Animals; D000917:Antibody Formation / Q000187:drug effects*; D000921:Antibody-Producing Cells / Q000187:drug effects / Q000276:immunology*; D003513:Cycloheximide / Q000494:pharmacology; D004912:Erythrocytes / Q000276:immunology; D006462:Hemolytic Plaque Technique; D006801:Humans; D051379:Mice; D011433:Propranolol / Q000494:pharmacology; D012217:Rheumatoid Factor / Q000096:biosynthesis*; D013154:Spleen / Q000276:immunology; D014747:Vinblastine / Q000494:pharmacology
D014747:Vinblastine; D012217:Rheumatoid Factor; D003513:Cycloheximide; D011433:Propranolol