{'fraction_non_alphanumeric': 0.03309029725182277, 'fraction_numerical': 0.0179472798653954, 'mean_word_length': 5.006734006734007, 'pattern_counts': {'":': 0, '<': 2, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Elevated interleukin-10 levels in patients with rheumatoid arthritis.

OBJECTIVE
Interleukin-10 (IL-10) has been shown to exert both antiinflammatory and immunostimulatory effects in vivo and in vitro. We therefore sought to examine the role of this cytokine in rheumatoid arthritis (RA) by assessing serum and synovial fluid IL-10 levels.


METHODS
Serum and synovial fluid samples were collected from patients with RA and patients with various inflammatory, infectious, and noninflammatory arthritides (controls). IL-10 was assayed using an IL-10-specific enzyme-linked immunosorbent assay, and messenger RNA (mRNA) levels were assessed by semi-quantitative polymerase chain reaction (PCR) techniques.


RESULTS
Both RA serum and synovial fluid contained significantly elevated IL-10 levels compared with levels in normal subjects or in control patients (P < 0.01). Some patients with spondylarthropathy also manifested increased serum levels of IL-10. Serum levels of IL-10 did not correlate with standard measures of clinical activity, but were shown to correlate significantly with serum rheumatoid factor (RF) titers and in vitro levels of spontaneous IgM-RF production (P < 0.05). PCR analyses demonstrated the constitutive expression of IL-10 mRNA by the non-T cell population, and semiquantitative PCR analysis documented elevated levels of IL-10 mRNA in circulating mononuclear cells of those RA patients who were not treated with slow-acting antirheumatic drugs. Analysis of IL-10 mRNA revealed the cytokine to be of human, and not viral, origin.


CONCLUSION
These data suggest that there is increased production of IL-10 by non-T cells in patients with RA. This may contribute to the diminished T cell function and increased antibody and RF production in these patients.