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Altered interleukin‐2 secretion in patients with primary fibromyalgia syndrome
Author(s) -
Hader Nader,
Rimon David,
Kinarty Amalia,
Lahat Nitza
Publication year - 1991
Publication title -
arthritis & rheumatism
Language(s) - English
Resource type - Journals
eISSN - 1529-0131
pISSN - 0004-3591
DOI - 10.1002/art.1780340712
Subject(s) - fibromyalgia , secretion , endocrinology , concanavalin a , medicine , cd8 , interleukin 2 , phorbol , interleukin , chemistry , immunology , protein kinase c , cytokine , kinase , immune system , in vitro , biochemistry
Interleukin‐2 (IL‐2) production was studied in T lymphocytes and isolated CD4+ T lymphocytes from 12 patients with primary fibromyalgia syndrome and 10 healthy volunteers. The dose and time kinetics of IL‐2 production by concanavalin A‐stimulated T cells and CD4+ T cells of fibromyalgia patients differed from findings in controls by 1) a need for a higher concentration of mitogen in order to achieve optimal IL‐2 secretion, and 2) a delay in the peak time of optimal IL‐2 secretion. Unlike normal IL‐2 secretion, which was higher after removal of CD8+ T cells, the pattern and degree of IL‐2 secretion by cells from fibromyalgia patients were not changed following removal of CD8+ T cells. Addition of calcium ionophore in assays using suboptimal concanavalin A concentrations did not correct the reduction in IL‐2 secretion by fibromyalgia patient T cells, but addition of phorbol myristate acetate induced normal secretion of IL‐2. These findings suggest that there is a defect in the IL‐2 pathway, which is related to protein kinase C activation and does not involve impairment of Ca 2+ elevation, in patients with fibromyalgia.

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