Abstract
Background
Interleukin 35 (IL-35) is likely to contribute to the development of autoimmune diseases,
as the Epstein-Barr virus- induced gene protein 3 (EBI3) is the specificity subunit
of IL-35. Nevertheless, until recently, no studies have evaluated its role in systemic
lupus erythematosus (SLE) in humans. The objective of this study was to investigate
the serum IL-35 level and the percentage of CD4+EBI3+ T cells in the peripheral blood of patients with SLE and explore the roles of double-positive
T cells and IL-35 in the pathogenesis of SLE and the effects of glucocorticoid on
these roles.
Methods
Fifty-five hospitalized patients with SLE were recruited, and 20 volunteers were enrolled
as healthy controls. Serum IL-35 levels were measured by enzyme-linked immunosorbent
assay, and the percentage of CD4+EBI3+ T cells was analyzed by flow cytometry.
Results
The serum IL-35 level and the percentage of CD4+EBI3+ T cells were significantly decreased in patients with active SLE compared with healthy
controls and patients with inactive SLE. The serum IL-35 level and the percentage
of CD4+EBI3+ T cells were negatively correlated with the SLE disease activity index. The percentages
of CD4+EBI3+ T cells and serum IL-35 levels in 10 untreated patients with active SLE were increased
at days l, 3, and 7 after the treatment with methylprednisolone (0.8 mg-kg−1-d−1) compared with the percentages before the treatment.
Conclusions
These results demonstrate that abnormalities in IL-35 and CD4+EBI3+ T cells may play important roles in the pathogenesis of SLE; the percentage of double-positive
T cells and the level of IL-35 are parameters for the evaluation of SLE activity and
severity.
Key Indexing Terms
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Article info
Publication history
Accepted:
October 4,
2013
Received:
May 31,
2013
Footnotes
This study was partially supported by the National Natural Science Foundation of China (Grant No. 81200507).
The authors have no financial or other conflicts of interest to disclose.
Identification
Copyright
© 2013 Southern Society for Clinical Investigation. Published by Elsevier Inc. All rights reserved.
