Session Information
Session Type: Abstract Submissions (ACR)
Background/Purpose: Regulatory IL-10 producing B cells (B10) have been shown to prevent and cure collagen-induced arthritis in mice. In human, very little is known about B10 cells in rheumatoid arthritis (RA). Several B cell subsets such as CD24hiCD38hi, CD24hiCD27+ and CD5+ B cells were suggested to be precursors of B10 cells. In the present study, we aimed to analyze these B cell subsets and B10 cells in RA patients and healthy controls. We also compared the ability of these different B cell subsets to produce IL-10.
Methods: B10 cells were generated from PBMCs stimulated for 24 hours with CpG and 4 hours with PMA and ionomycine. Intra-cellular B cell IL-10 was assessed by cytometry. Thirty-one controls + 99 RA patients were included for B cell subsets and 21 controls + 66 RA patients for B10 cell assessment. To study the ability of the different B cell subsets to produce IL-10, we sorted them using cytometry before activation.
Results: After multiple adjustments, CD24hiCD38hi, CD24hiCD27+ and CD5+ B cell levels were found to be similar in patients with RA and in controls. CD24hiCD27+ levels were higher in patient with active disease than in patient with DAS28≤3.2 whereas other subsets were not different between the two groups. Levels of B10 cells were lower in patients with RA, especially in RA with disease duration under 5 years than controls. B10 cells inversely correlated with DAS28. It was more pronounced in RA≤5 years where B10 cells also inversely correlated with CRP levels. Moreover, B10 cells inversely correlated with rheumatoid factor and anti-citrullinated peptide antibody levels. CD24hiCD27+ B cells were found to be the main producers of IL-10 when taking into account their percentage in peripheral blood. However, all B cell subsets were able to produce more or less IL-10 after stimulation.
Conclusion: B cell ability to produce IL-10 was altered in RA and this impairment influenced disease activity, biological inflammation and auto-antibody levels, especially in patients with RA≤5 years. This strongly suggests a role of B10 cells in RA initiation.
Disclosure:
C. I. Daien,
None;
S. Gailhac,
None;
T. Mura,
None;
B. Combe,
Merck,
2,
Pfizer Inc,
2,
Roche-Chugai,
2,
Merck Human Health,
5,
Pfizer Inc,
5,
Roche-Chugai,
5,
UCB Pharma,
5,
Bristol-Myers Squibb,
5,
Celgene,
5,
Lilly,
5,
Novartis,
5,
Merck,
8,
Pfizer Inc,
8,
Roche-Chugai,
8,
UCB Pharma,
8,
Bristol-Myers Squibb,
8,
Celgene,
8,
Lilly,
8,
Novartis,
8;
M. Hahne,
None;
J. Morel,
Pfizer Inc,
2,
Bristol-Myers Squibb,,
5,
Abbott Laboratories,
5,
Pfizer Inc,
5,
Roche Pharmaceuticals,
5,
Merck Pharmaceuticals,
5.
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