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别嘌醇可降低人 T 细胞的抗原特异性和多克隆活化。

Allopurinol reduces antigen-specific and polyclonal activation of human T cells.

机构信息

Instituto Nacional de Parasitología "Dr. Mario Fatala Chaben" Ciudad Autónoma de Buenos Aires, Argentina.

出版信息

Front Immunol. 2012 Sep 21;3:295. doi: 10.3389/fimmu.2012.00295. eCollection 2012.

DOI:10.3389/fimmu.2012.00295
PMID:23049532
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3448060/
Abstract

Allopurinol is the most popular commercially available xanthine oxidase inhibitor and it is widely used for treatment of symptomatic hyperuricaemia, or gout. Although, several anti-inflammatory actions of allopurinol have been demonstrated in vivo and in vitro, there have been few studies on the action of allopurinol on T cells. In the current study, we have assessed the effect of allopurinol on antigen-specific and mitogen-driven activation and cytokine production in human T cells. Allopurinol markedly decreased the frequency of IFN-γ and IL-2-producing T cells, either after polyclonal or antigen-specific stimulation with Herpes Simplex virus 1, Influenza (Flu) virus, tetanus toxoid and Trypanosoma cruzi-derived antigens. Allopurinol attenuated CD69 upregulation after CD3 and CD28 engagement and significantly reduced the levels of spontaneous and mitogen-induced intracellular reactive oxygen species in T cells. The diminished T cell activation and cytokine production in the presence of allopurinol support a direct action of allopurinol on human T cells, offering a potential pharmacological tool for the management of cell-mediated inflammatory diseases.

摘要

别嘌醇是最常见的黄嘌呤氧化酶抑制剂，广泛用于治疗症状性高尿酸血症或痛风。虽然别嘌醇在体内和体外都显示出了几种抗炎作用，但关于其对 T 细胞的作用的研究较少。在本研究中，我们评估了别嘌醇对人 T 细胞中抗原特异性和有丝分裂原驱动的激活以及细胞因子产生的影响。别嘌醇明显降低了 T 细胞产生 IFN-γ 和 IL-2 的频率，无论是在用单纯疱疹病毒 1、流感病毒、破伤风类毒素和克氏锥虫衍生抗原进行多克隆或抗原特异性刺激后。别嘌醇减弱了 CD3 和 CD28 结合后 CD69 的上调，并显著降低了 T 细胞中自发和有丝分裂原诱导的细胞内活性氧水平。别嘌醇存在时 T 细胞激活和细胞因子产生减少支持别嘌醇对人 T 细胞的直接作用，为细胞介导的炎症性疾病的管理提供了一种潜在的药理学工具。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9d11/3448060/8f1ddb3a031c/fimmu-03-00295-g0006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9d11/3448060/1860b5891791/fimmu-03-00295-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9d11/3448060/cb3b2eac136a/fimmu-03-00295-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9d11/3448060/5a826272ca53/fimmu-03-00295-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9d11/3448060/b2f91c6cb30a/fimmu-03-00295-g0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9d11/3448060/51d4b2108e4e/fimmu-03-00295-g0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9d11/3448060/8f1ddb3a031c/fimmu-03-00295-g0006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9d11/3448060/1860b5891791/fimmu-03-00295-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9d11/3448060/cb3b2eac136a/fimmu-03-00295-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9d11/3448060/5a826272ca53/fimmu-03-00295-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9d11/3448060/b2f91c6cb30a/fimmu-03-00295-g0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9d11/3448060/51d4b2108e4e/fimmu-03-00295-g0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9d11/3448060/8f1ddb3a031c/fimmu-03-00295-g0006.jpg

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