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目的研究适应性调节性T细胞(iTreg细胞)在系统性红斑狼疮(SLE)病理机制中的作用。方法根据SLE疾病活动度(SLEDAI)评分,将35例SLE患者(D组)分为非活动组(A组,12例)和活动组(B组,23例);另选取22例健康志愿献血者为正常对照组(C组)。用CD3抗体、CD28抗体、转化生长因子β(TGF-β)和IL-2诱导外周血CD4~+CD25~-T细胞,流式细胞术检测诱导转化获得的CD4+CD25+Foxp3+T细胞转化率、TGF-β受体和IL-2受体表达,并分析其与SLEDAI评分的相关性。结果与C组相比,B组CD4~+CD25~-T细胞经诱导后的CD4+CD25+T细胞比例降低[(9.74±20.50)%vs.(95.85±3.81)%](P<0.01)。D组诱导转化形成的iTreg细胞比例低于C组(P<0.01),且与SLEDAI评分呈负相关(r=-0.77,P<0.05)。D组CD4~+CD25~-T细胞中IL-2受体γ链表达低于C组(P<0.05),且与SLEDAI评分呈负相关(r=-0.66,P<0.05)。D组CD4~+CD25~-T细胞中TGF-β受体Ⅰ表达高于C组(P<0.05),但与SLEDAI评分无相关性(r=-0.27,P>0.05)。结论 SLE患者IL-2受体γ链表达缺陷所导致的IL-2受体信号受损可能引起iTreg细胞诱导形成障碍,从而参与SLE的发病机制。
Objective To study the role of adaptive regulatory T cells (iTregs) in the pathogenesis of systemic lupus erythematosus (SLE). Methods Thirty-five SLE patients (group D) were divided into inactive group (group A, n = 12) and active group (group B, n = 23) according to SLE disease activity score For the normal control group (C group). Peripheral blood CD4 ~ + CD25 ~ -T cells were induced by CD3 antibody, CD28 antibody, transforming growth factor β (TGF-β) and IL-2. Flow cytometry was used to detect the transformation of CD4 + CD25 + Foxp3 + T cells Rate, TGF-beta receptor and IL-2 receptor expression, and analyzed their association with the SLEDAI score. Results Compared with group C, the proportion of CD4 + CD25 + T cells in group B was significantly lower than that in group C (9.74 ± 20.50 vs 95.85 ± 3.81%, P <0.01) . The proportion of iTreg cells induced by D group was lower than that of C group (P <0.01), and negatively correlated with SLEDAI score (r = -0.77, P <0.05). The expression of IL-2 receptor γ chain in CD4 ~ + CD25 ~ -T cells in group D was lower than that in group C (P <0.05), and negatively correlated with SLEDAI score (r = -0.66, P <0.05). The expression of TGF-β receptor I in CD4 ~ + CD25 ~ -T cells in group D was higher than that in group C (P <0.05), but not with SLEDAI score (r = -0.27, P> 0.05). Conclusions The impaired IL-2 receptor signaling induced by deficient expression of IL-2 receptor γ chain in SLE patients may lead to the formation of impaired induction of iTreg cells, which may be involved in the pathogenesis of SLE.