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Immunological Characterization of Lymphocytes in Synovial Fluid from Patients with Rheumatoid Arthritis
Author(s) -
FRφLAND S. S.,
NATVIG J. B.,
HUSBY G.
Publication year - 1973
Publication title -
scandinavian journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.934
H-Index - 88
eISSN - 1365-3083
pISSN - 0300-9475
DOI - 10.1111/j.1365-3083.1973.tb02017.x
Subject(s) - synovial fluid , rheumatoid arthritis , synovial membrane , lymphocyte , immunology , pathogenesis , medicine , peripheral , peripheral blood , pathology , chemistry , alternative medicine , osteoarthritis
Lymphocytes separated from synovial fluid in rheumatoid arthritis by means of gradient centrifugation were characterized with regard to B‐ and T‐lymphocyte properties. Membrane‐bound Ig detectable with immunofluorescence technique was utilized as a marker of B‐lymphocytes, while the ability to bind sheep erythrocytes and form rosettes was interpreted as a T‐lymphocyte characteristic. In 9 out of 18 patients studied no Ig‐positive lymphocytes were found in synovial fluid, while the remaining 9 patients had 1% or less. Appropriate control experiments indicated that the absence of membrane‐bound Ig on lymphocytes was not due to in vivo induced redistribution with subsequent endocytosis of Ig receptors. The percentages of B‐lymphocytes in peripheral blood from patients (mean 11% and range 3–19%) were not significantly different from those of 54 normal individuals (mean 10% and range 3–22%). Rosette‐forming lymphocytes were found in synovial fluid of 11 patients studied, with mean 29.6% and range 19.0–60.2%, which are significantly higher than the corresponding values in peripheral blood, 22.7% and 0.9–41.1%. The latter values were also significantly higher than those of peripheral blood from 32 normals (mean 14.8% and range 0.9–34.7%). The increased proportions of T‐lymphocytes in synovial fluid in rheumatoid arthritis in contrast to the absence or very low numbers of B‐lymphocytes may indicate an important role for the former in the pathogenesis of rheumatoid inflammation.