Addition of propranolol to the agarose phase of a plaque-forming cell (PFC) assay for rheumatoid factor (RF) caused reduction in the number of plaques seen. This reduction in rheumatoid factor plaque-forming cell ( R F PFC) did not depend upon an effect at the 8-adrenergic receptor, since d-and I-propranolol reduced equally well. Furthermore, in a series of polycyclic compounds with varying &receptor blocking capabilities there was no agreement between plaque reduction and blocking. When propranolol was tested in the agarose in an anti-sheep erythrocyte (SRC) plaque assay (anti-SRC PFC), it had no inhibitory effect, but it was capable of inhibiting the generation of new anti-SRC PFC in an in vitro culture. Propranolol is thought to exert these effects through its membrane stabilizing (anesthetic) properties.
E. ROSE, and JOHN H. VAUGHANThe production and release of rheumatoid factor (RF) by lymphoid cells of certain patients with rheumatoid arthritis (RA) have been shown in bone marrows, synovial fluids, and peripheral bloods by a hemolytic plaque-forming cell ( R F PFC) assay (1). The target cells used were sheep cells sensitized with reduced and alkylated rabbit IgG antibody, which lysed directly in the presence of added rheumatoid factor plus complement. Dependence of the R F PFC on protein synthesis and intact microtubular excretory system was indicated by studies in which cycloheximide or vinblastine was added to the agar. In other studies the addition of propranolol also markedly reduced the number of R F PFC observed. This effect of propranolol did not seem to be explained on the basis of its ability to block 6-adrenergic receptors. This study was designed to learn more about the propranolol effect.
MATERIALS AND METHODSSubjects. The human lymphocytes studied were from normal laboratory personnel or from patients with seropositive RA, high numbers of R F PFC in their blood, and erythrocyte sedimentation rates greater than 40 mm per hour.Fifty to 250 ml of each patient's blood were drawn into heparinized syringes and allowed to sediment for an hour. The leukocyte-rich plasma and top 10-20% of red cells were expressed into separate tubes and the remaining red cells then returned to the patients by intravenous infusion.Preparation of Lymphocytes from Patients. The leukocyte-red cell suspension was diluted 1 :2 in normal saline and layered in 30 ml aliquots over 12 ml of ficoll-hypaque (2).
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