Abstract
BackgroundSystemic lupus erythematosus (SLE) is a prototypic systemic autoimmune disease. Complement component 4 (C4) has be proved to play a role in pathogenesis of SLE. In the present study, we investigated the effect of C4 on T cells differentiation.MethodsThirty SLE patients were included in this study. CD4+ T cells were isolated from healthy subjects, and dendritic cells (DCs) were isolated from healthy subjects or SLE patients. C4 was supplemented to co-incubate with T cells and DCs.ResultsSerum C4 concentration was positively correlated with regulatory T cell (Treg) percentage (R2 = 0.5907, p < 0.001) and TGFβ concentration (R2 = 0.5641, p < 0.001) in SLE patients. Different concentrations of C4 had no effect on T cells differentiation. Co-incubated T cells with DCs and C4 for 7 days, the Treg percentage and TGF-β concentration were significantly elevated. In addition, pre-treated DCs (from healthy subjects or SLE patients) with C4 and then co-incubated with T cells, the increases of Treg percentage and TGF-β concentration were also observed.ConclusionC4 takes part in T cells differentiation to Treg cells via DCs.
Highlights
Systemic lupus erythematosus (SLE) is a prototypic systemic autoimmune disease
Summary of study group characteristics and observed expressions As shown in Table 1, the patients with com‐ ponent 4 (C4) copy numbers 4 for sample number, and there were no significant differences in age, gender and duration of disease among three groups
Serum complement C4 concentrations were elevated with the increasing of C4 copy numbers
Summary
Systemic lupus erythematosus (SLE) is a prototypic systemic autoimmune disease. Complement com‐ ponent 4 (C4) has be proved to play a role in pathogenesis of SLE. Systemic lupus erythematosus (SLE), a severe multisystem autoimmune disease, is characterized by a loss of immune tolerance to self-antigens (Ags), which results in the persistent production of pathogenic autoantibodies, activation of lymphocyte and release of inflammatory mediators [1]. Environmental and hormonal contribute to initiate and drive SLE pathogenesis [2]. The definitive role of Treg cells in SLE remains not fully clear. In SLE patients, the reduced number and function of CD4+CD25 Foxp Tregs have been observed [6]. The deficiencies of Tregs might contribute to the breakdown of self-tolerance and the development of the autoimmune response in SLE patients [7]
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