Interleukin-2 (IL-2) receptor bearing cells and soluble IL-2, measured in a bioassay with IL-2 dependent human T-cell blasts, were recognized in synovial fluid, but not in the peripheral blood of patients with rheumatoid arthritis (RA). After stimulation in vitro with appropriate concentrations of the mitogen concanavalin A (Con-A), comparable proportions of IL-2 receptor (IL-2R) bearing cells were seen in cultures of synovial fluid lymphocytes (SFL) and in cultures of peripheral blood lymphocytes (PBL). On the other hand, higher levels of secreted IL-2 were found in SFL cultures compared to corresponding PBL cultures of RA patients and normal donors. Specificity of the IL-2 bioassay was confirmed by blocking the T-cell blast proliferation (induced by SFL culture supernatants), by 83 +/- 4%, after addition of a monoclonal anti-IL-2R antibody. Despite the high levels of soluble IL-2, only a weak proliferative response was observed in the corresponding SFL cultures.
SUMMARY
Mononuclear cells from peripheral blood (PBMC) of rheumatoid arthritis (RA) patients and healthy controls were incubated with α‐CD3. Cytokine secretion from 2h to 72 h of incubation was measured by ELISA, There were no significant differences in secretion of T cell derived IL‐2 and IL‐4 in cultures from RA patients and controls. The macrophage‐derived cytokines, IL‐1β and tumour‐necrosis factor‐α (TNF‐α) were secreted with a steep increase of concentration during the first 16 h of incubation by PBMC from RA patients. PBMC from healthy controls secreted both cytokines at a constantly rising rate with a maximum for TNF‐α at 48 h and for IL‐1β at 72 h. Interferon‐γ (IFN‐γ) is secreted in significantly reduced concentrations by PBMC from untreated RA patients compared with controls. Gold‐salt treatment led to a slightly delayed and enhanced secretion of TNF‐α and IL‐1β, an enhanced secretion of IL‐2 and a restored secretion of IFN‐γ.
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