Abstract
The apoptotic signaling pathway is obviously disordered in systemic lupus erythematosus (SLE). Natural IgM (nIgM) is important in clearing apoptotic cells and preventing them from triggering deleterious autoimmunity. B-1 and innate-like B (ILBs) cells are the main nIgM producers. Human CD27+IgD+ B cells (un-switched memory B cells) are considered ILBs. However, their functional properties in SLE remain undefined. Peripheral blood sample of 50 SLE patients and 50 healthy controls were collected, and twelve SLE patients were assessed in a follow-up study. The amount of CD27+IgD+ B cell in each population was analyzed by flow cytometry. The IgM and IL-10 levels of CD27+IgD+ B cell were assessed by ELISPOT and qRT-PCR, respectively. SPSS 17.0 (SPSS, USA) was employed for data analysis. P < 0.05 indicated statistical significance. The amounts of CD27+IgD+ B cell were significantly decreased in SLE patients than healthy control (P < 0.01). CD27+IgD+ B cell amounts were positively correlated with WBC (r = 0.337, P = 0.017), platelet count (r = 0.396, P = 0.004), and serum C3 levels (r = 0.415, P = 0.003) and negatively correlated with serum creatinine levels (r = - 0.285, P = 0.045), SLEDAI(r = - 0.724, P = 0.000), and anti-dsDNA(r = - 0.477, P = 0.000). The IgM and IL-10 levels of CD27+IgD+ B in active SLE were decreased than healthy control (P < 0.001). Moreover, CD27+IgD+ B cells are increased in SLE cases after treatment than before treatment (P < 0.001). The amounts of CD27+IgD+ B cell were significantly decreased in SLE patients compared with the healthy population, and CD27+IgD+ B cell was verified to be correlated with clinical and immunological features in SLE patients. CD27+IgD+ B cells had impaired function associated with IgM and IL-10 production in active SLE. Moreover, the amounts of CD27+IgD+ B cells were recovered to the normal level in SLE cases with treatment-related disease remission. Key Points • CD27+IgD+ B cell amounts are significantly decreased in SLE patients than healthy control. • CD27+IgD+ B cells are functionally impaired in producing natural antibody-like IgM and IL-10 in SLE patients. • CD27+IgD+ B cell amounts are correlated with clinical and immunological features in SLE.
Highlights
Systemic lupus erythematosus (SLE), a major systemic autoimmune disorder, affects humans with genetic susceptibility in certain environmental conditions[1]
To examine the function of CD27+IgD+B cells in systemic lupus erythematosus (SLE) pathogenesis, their amounts were firstly compared between SLE and healthy control (HC) patients
The 50 HCs showed remarkably higher circulatory CD27+IgD+B cell amounts compared with the 50 individuals with SLE (Figure 1B and C)
Summary
Systemic lupus erythematosus (SLE), a major systemic autoimmune disorder, affects humans with genetic susceptibility in certain environmental conditions[1]. Antibodies could harm self-tissues via complement-mediated inflammatory reactions, programmed cell death and immune-complexes associated injury. The exact role of antibodies in SLE remains unraveled[2]. It has been demonstrated that the apoptosis signaling pathway is obviously disordered in SLE. Abnormal production of a large number of apoptotic signaling molecules, including TNF-related apoptosis inducing ligand (TRAIL), TNF-like weak inducer of apoptosis (TWEAK) and death ligand FasL (Fas ligand), leads to abnormal increase of apoptosis[4, 5]. Cell death (programmed cell death, necrosis and NETosis [affecting neutrophils via NETs]), provides most of the self-dsDNA that induces immune reactions and causes autoimmune disorders[6]
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