Drugs affecting the release of rheumatoid factor in a plaque‐forming cell assay

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 (RF PFC) did not depend upon an effect at the β‐adrenergic receptor, since d‐ and l‐pro...

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Bibliographic Details
Published in:Arthritis and rheumatism 1978-01, Vol.21 (1), p.114-119
Main Authors: Moore, Terry L., Robbins, Dick L., Rose, Jean E., Vaughan, John H.
Format: Article
Language:English
Subjects:
Adrenergic beta-Antagonists
Cell Membrane
Hemolytic Plaque Technique
Humans
Immunosuppressive Agents
Propranolol - pharmacology
Receptors, Adrenergic - drug effects
Rheumatoid Factor - biosynthesis
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Summary: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 (RF PFC) did not depend upon an effect at the β‐adrenergic receptor, since d‐ and l‐propranolol reduced equally well. Furthermore, in a series of polycyclic compounds with varying β‐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.
ISSN:0004-3591
1529-0131
DOI:10.1002/art.1780210118