Front Immunol：pConsensus Peptide (pCons)诱导的狼疮CD8+和CD4+调节性T细胞的细胞和分子表型

2022-01-21 从医路漫漫 MedSci原创

系统性红斑狼疮是一种慢性自身免疫性疾病，调节性T细胞(Treg)在包括SLE在内的许多炎症性和自身免疫性疾病中具有保护作用。

系统性红斑狼疮(Systemic lupus erythematosus, SLE)是一种慢性自身免疫性疾病，调节性T细胞(T_reg)在包括SLE在内的许多炎症性和自身免疫性疾病中具有保护作用。对异常免疫调节的调节是自身免疫性疾病的研究的对象。治疗的目标是通过恢复免疫系统的自我耐受来限制异常致病细胞和自身抗体的数量和活性。一种方法是通过给药肽(如pConsensus肽，依拉肽和核小体肽)来诱导调节性T细胞。另一种方法是利用纳米颗粒扩大调节性T细胞以治疗自身免疫性疾病，包括狼疮。尽管调节性CD4⁺T细胞的数量和/或功能的减少在SLE中已经被广泛研究，但CD8⁺T_reg亚群的作用和特征尚不清楚。研究CD8⁺T_reg细胞功能活动和存活的基因、调控网络和信号通路，对于开发SLE和其他自身免疫性疾病中恢复免疫稳态的治疗方法很重要。然而，为了合理干预并恢复免疫稳态，CD8⁺T_reg分化、扩张、维持和调节功能的分子表型、机制和途径仍有待进一步了解。

我们开发了一种独特的模型，在狼疮动物模型(NZB/NZW) F1 (BWF1)小鼠中诱导CD8⁺调节性T细胞抑制自身免疫性疾病的发展。在这个模型中，我们已经表明,合成肽(pCons)基于T细胞的免疫球蛋白g VH地区因素对小鼠进行编码DNA抗体结合MHC I / II类地区可以激活CD8⁺ T细胞体外,这会抑制CD4 ⁺T辅助细胞和B细胞活动。此外，当pCons在体内使用时，我们证明了抗DNA抗体的产生受到抑制，并导致肾炎。然而，pCon诱导的CD8⁺调节性T细胞的细胞和分子表型尚不完全清楚。在本研究中，我们进一步提供了新的信息，定义了pCon诱导的CD8⁺T调节性细胞和CD4⁺调节性T细胞的免疫学和分子表型。我们还发现pCons治疗降低了CD4⁺T细胞、CD8⁺T细胞和B220⁺B细胞的凋亡。此外，我们发现pCons也能诱导健康人外周血单个核细胞(pmcs)中CD8⁺FoxP3⁺Treg细胞。

在本研究中，我们进一步研究了pCon诱导的CD4⁺和CD8⁺ T_reg亚群的分子和细胞表型。流式细胞术分析显示，pCons诱导CD8+T_reg细胞的细胞表面分子有以下几个:CD25^highCD28^high^and^l^ow^subsets(如前面所示)、CD62L^high、CD122^low、PD1^low、CTLA4^low、ccr7^low和41BB^high。qRT-PCR (Quantitative real-time PCR)基因表达分析显示，pcons诱导的CD8+T_regcells下调了以下几个基因:G蛋白信号转导调控因子(Regulator of G protein signaling, RGS2)、RGS16、RGS17、BAX、GPT2、PDE3b、GADD45β和程控细胞死亡1 (PD1)。进一步，我们在蛋白质水平上通过Western blot分析证实了这些基因的下调。

我们发现pCons显著提高了CD8⁺FoxP3⁺T细胞的百分比，并进一步提高了FoxP3的平均荧光强度(MFI)，健康外周血单个核细胞(pmcs)被pCons (10mg/ml, 24-48小时)处理。此外，我们还发现pCons降低了BWF1狼疮小鼠CD4⁺、CD8⁺T细胞和B220⁺B细胞的凋亡。

这些数据表明pCons刺激调节性T细胞的细胞、免疫和分子变化，从而保护对抗SLE自身免疫。

原文出处：Singh RP, Hahn BH, Bischoff DS,Cellular and Molecular Phenotypes of pConsensus Peptide (pCons) Induced CD8 and CD4 Regulatory T Cells in Lupus.Front Immunol 2021;12

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2022-12-06 xuyu

#CD4+#

39 0
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2022-06-20 qidongfanjian

#CD4#

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2022-06-13 feather89

#PE#

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2022-01-21 查查佳佳

统性红斑狼疮(Systemic lupus erythematosus, SLE)是一种慢性自身免

56 0
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2022-01-19 sunrural_42825357

#狼疮#

29 0
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2022-01-19 tastas

#表型#

29 0
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2022-01-19 ms691033630344116

#CD8#

42 0

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