Abstract
Systemic lupus erythematosus (SLE) is a multisystemic autoimmune disease that is associated with the destruction of immune tolerance and activation of B cells. Interleukin (IL)-35 and IL-35-producing (IL-35+) regulatory B cells (Bregs) have been demonstrated to possess immunosuppressive functions, but their roles in the initiation and early development of SLE have not been explored. Here, we measured and compared the frequencies of blood regulatory B cell subsets and the concentrations of plasma IL-35, IL-10, IL-17A, tumor necrosis factor (TNF)-α, and interferon (IFN)-γ in 47 Chinese patients with newly diagnosed SLE and 20 matched healthy controls (HCs). The SLE patients had decreased percentages of IL-35+ B cells and IL-10+ B cells among the total blood B cells as well as decreased concentrations of plasma IL-35. In addition, higher levels of plasma IL-10, IFN-γ, TNF-α, and IL-17 along with higher frequencies of circulating plasma and memory B cells were observed in the SLE patients. The percentage of IL-35+ Bregs and the serum IL-35 level were inversely correlated with the SLE disease activity index and the erythrocyte sedimentation rate (ESR) levels. Our results indicate that IL-35+ Bregs and IL-35 may play protective roles in SLE initiation and progression.
Highlights
Systemic lupus erythematosus (SLE) is a chronic inflammatory autoimmune disease featured with high amounts of autoantibody production and systemic clinical manifestations, including fatigue, joint pain, rash, and fever[1]
Our results demonstrated that the percentages of IL-35+ Bregs (P = 0.0039, r = −0.4130; Fig. 6A) and IL-10+ Bregs (P = 0.0026, r = −0.4294; Fig. 6C) as well as the plasma IL-35 levels (P = 0.0053, r = −0.4004; Fig. 6E) were inversely correlated with the SLE Disease Activity Index (SLEDAI) scores of the SLE patients
Our study indicated that the frequency of the CD27+CD38+ plasma B cell subset was positively correlated with the SLEDAI score (P = 0.0016, r = 0.4485; Fig. 7A) as well as the concentrations of C-reactive protein (CRP) (P = 0.0219, r = 0.3372; Fig. 7B) and IgA (P = 0.0286, r = 0.3379; Fig. 7C) in the new-onset SLE patients
Summary
Systemic lupus erythematosus (SLE) is a chronic inflammatory autoimmune disease featured with high amounts of autoantibody production and systemic clinical manifestations, including fatigue, joint pain, rash, and fever[1]. A B cell subset, namely regulatory B cells (Bregs), has been revealed to possess immunosuppressive functions and support immunological tolerance[4,5]. In autoimmune diseases including SLE and rheumatoid arthritis, IL-10-producing (IL-10+) Bregs have been shown to be functionally impaired and decreased in numbers[6,8,9]. IL-35 and IL-35+ Bregs have recently been confirmed to be important players in mediating immune tolerance in patients with autoimmune diseases. We measured the concentrations of plasma cytokines, including IL-35, IL-10, IL-17, tumor necrosis factor (TNF)-α, and interferon (IFN)-γ, and further evaluated their correlations among the abundances of the Breg subsets, the concentrations of plasma cytokines, and other clinical indicators of SLE patients
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