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Decreased Catecholamine‐Induced Cell Death in B Lymphocytes from Patients with Rheumatoid Arthritis
Author(s) -
WAHLE M.,
PIERER M.,
KRAUSE A.,
KÖLKER S.,
BAERWALD C.G. O.
Publication year - 2002
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1111/j.1749-6632.2002.tb04243.x
Subject(s) - rheumatoid arthritis , propidium iodide , agonist , endocrinology , medicine , stimulation , apoptosis , pathogenesis , annexin , programmed cell death , receptor , isoprenaline , lymphocyte , arthritis , immunology , biology , flow cytometry , biochemistry
A bstract : The expression of β 2 ‐adrenergic receptors (β 2 ‐R) on B lymphocytes and agonist‐induced cAMP production is reduced in patients with rheumatoid arthritis (RA). To further study functional consequences of the diminished β 2 ‐R density on B lymphocytes in RA patients, agonist‐induced cell death was evaluated and compared to healthy controls. B lymphocytes from patients with RA and healthy controls were activated with anti‐IgM‐antibody. Coincubation was carried out with isoprenaline (iso, 0.001‐10 μM). Apoptotic and necrotic cells were determined using Annexin‐V and propidium‐iodide staining. β 2 ‐R‐induced cell death in B cells from healthy volunteers was stimulated after 24 h (medium, 21.2 ± 1.6%; iso, 34.6 ± 4.4%; increase 59.3 ± 10.1%). However, in RA patients the increase in cell death following β 2 ‐R stimulation (21.8 ± 8.9%) was significantly impaired ( p = 0.02 ). Our data demonstrate that catecholamine‐induced cell death after stimulation of β 2 ‐R on B lymphocytes is decreased in RA patients, possibly contributing to the pathogenesis of the disease.