וֹndoleamine-2,3-dioxygenase (IDO) plays a role in immune regulation. Increased IDO activity was reported in systemic lupus erythematosus (SLE). We investigated the effects of the tolerogenic peptide hCDR1, shown to ameliorate lupus manifestations, on IDO gene expression. mRNA was prepared from splenocytes of hCDR1- treated SLE-afflicted (NZBxNZW)F1 mice, from blood samples of lupus patients, collected before and after their in vivo treatment with hCDR1 and from peripheral blood mononuclear cells (PBMC) of patients incubated with hCDR1. IDO gene expression was determined by real-time RT-PCR. hCDR1 significantly down-regulated IDO expression in SLE-affected mice and in lupus patients (treated in vivo and in vitro). No effects were observed in healthy donors or following treatment with a control peptide. Diminished IDO gene expression was associated with hCDR1 beneficial effects. Our results suggest that the hCDR1-induced FOXP3 expressing regulatory T cells in lupus are not driven by IDO but rather by other hCDR1 regulated pathways.

壬二胺-2,3-二加氧酶（IDO）在免疫调节中起作用。据报道，系统性红斑狼疮（SLE）的IDO活性增加。我们调查了耐受性肽hCDR1对IDO基因表达的影响，已证明其可以改善狼疮的表现。从hCDR1处理过的SLE受损（NZBxNZW）F1小鼠的脾细胞，狼疮患者的血样，在hCDR1体内治疗前后收集的mRNA以及从与hCDR1孵育的患者的外周血单个核细胞（PBMC）中制备mRNA。通过实时RT-PCR确定IDO基因表达。hCDR1显着下调了受SLE影响的小鼠和狼疮患者（体内和体外治疗）的IDO表达。在健康的供体中或在用对照肽治疗后未观察到效果。IDO基因表达减少与hCDR1的有益作用有关。我们的结果表明，hCDR1诱导的狼疮中表达FOXP3的调节性T细胞不是由IDO驱动，而是由其他hCDR1调节的途径驱动。