CD4＋CD25＋调节性T细胞在狼疮性肾炎中的变化及霉酚酸酯对其的影响

Effect of Mycophenolate Mofetii on the Change of CD4＋ CD25＋ Regulatory T Cells in Lupus Ne- phritis

【目的】观察CD4＋CD25＋调节性T细胞（Treg）及细胞因子在狼疮肾炎（LN）患者中表达的变化及霉酚酸酯（MMF）对其的影响。[A-法】将60例LN患者随机分为A、B两组，检测患者外周血CD4＋CD25＋Treg的百分率，测定白介素-2（IL-2）、白介素-10（1L-10）的表达，并与正常对照组（C组）进行对比。A组予激素加MMF、B组予以激素加环磷酰胺（cTX）诱导治疗6个月后再重复检测上述指标。【结果】A、B组治疗前CD4＋CD25＋Treg数量均显著低于C组，并伴有IL-2含量增高及IL-10含量降低，且差异均有显著性（P〈0．05）。A组治疗后CD4＋CD25＋Treg较前明显升高，IL-2含量下降，IL-10表达升高，且差异均有显著性（P〈0．05）。B组治疗后CD4＋CD25＋Treg数量、IL-10表达较治疗前无明显变化（P〉0．05），但IL-2含量下降，差异具有显著性（P〈0．05）。【结论】MMF在选择性抑制T、B淋巴细胞增殖的同时，可能通过上调CD4＋CD25＋Treg的数量及改善抗炎因子／促炎因子的失衡状态达到治疗LN等免疫性疾病的效果。

[Objective] To observe the change of CD4＋ CD25＋ regulatory T cell（Treg） and cytokines in patients with lupus nephritis（LN） and the effect of mycophenolate mofetil（MMF） on Tregs. [Methods] Totally 60 LN patients were randomly divided into group A and t3. The percentage of CD4＋ CD25＋ Treg in pe- ripheral blood of patients was detected. The expression of cytokines interleukin-2（IL-2） and interleukin-10（IL- 10） was measured and compared with control group（group C）. Group A was given hormones and MMF, while group B was given hormones and cyclophospbamide（CTX）. Above parameters were detected 6 months after treatment again. [Results] The percentage of CD4＋ CD25＋ Treg in group A and group before treatment was markedly lower than that in group C, and IL-2 increased and IL-10 decreased, and there was significant differ- ence（ P 〈0.05）. Compared before treatment, the percentage of CD4＋ CD25＋ Treg in group A after treatment increased, and IL-2 decreased and IL-10 increased, and there was significant difference（ P 〈0.05）. Compared with before treatment, the percentage of CD4＋ CD25＋ Treg and IL-10 in group B had no obvious change（ P〉 0.05）, but IL-2 decreased, and there was significant difference（ P 〈0.05）. [Conclusion] MMF can selectively inhibit the proliferation of T and 13 lymphocytes, and is effective for the treatment of LN and other autoim- mune diseases through up-regulating the number of CD4＋ CD25＋ Treg and rectifying the imbalance between proinflammatory cytokine/anti-proinflammatory. [-