Review Article

血红素加氧酶1在青少年自身免疫性疾病中的功能免疫调节作用

卷 19, 期 2, 2019

页: [110 - 116] 页: 7

弟呕挨: 10.2174/1566523219666190710092935

价格: $65

摘要

自身免疫疾病是一种炎症性疾病,其中人体的免疫系统攻击正常细胞,导致免疫功能降低和异常,最终导致组织损伤或器官功能障碍。在医学领域,尤其是儿科领域,关于自身免疫性疾病的知识仍然不足。一些常见的青少年自身免疫性疾病,如过敏性紫癜,全身性幼年特发性关节炎,粘膜皮肤淋巴结综合征和自身免疫性脑炎引起了公众的广泛关注。最近的研究表明,血红素加氧酶1(HO-1)是一种参与血红素降解的酶,在发病机制中起着关键作用,可能调节自身免疫。首先,它可以促进T淋巴细胞分化成CD4 + CD25 +调节性T细胞,并且可能与细胞因子(Th1 / Th2和Th17 / Treg)比例的变化有关。其次,HO-1可通过转化生长因子和白细胞介素等蛋白质的分泌来调节免疫系统。此外,增加HO-1的表达可以通过增加抗氧化剂水平来改善血管功能。因此,HO-1可为青少年自身免疫疾病的治疗管理提供理论依据和指导。

关键词: 青少年自身免疫性疾病,血红素加氧酶1,促炎细胞因子,炎性细胞因子,T淋巴细胞,MCLS。

图形摘要

[1]
Dunn LL, Midwinter RG, Ni J, Hamid HA, Parish CR, Stocker R. New insights into intracellular locations and functions of heme oxygenase-1. Antioxid Redox Signal 2014; 20(11): 1723-42.
[http://dx.doi.org/10.1089/ars.2013.5675]
[2]
Chen JC, Huang KC, Lin WW. HMG-CoA reductase inhibitors upregulate heme oxygenase-1 expression in murine RAW264.7 macrophages via ERK, p38 MAPK and protein kinase G pathways. Cell Signal 2006; 18(1): 32-9.
[http://dx.doi.org/10.1016/j.cellsig.2005.03.016] [PMID: 16214041]
[3]
Hamann CR, Egeberg A, Silverberg JI, Gislason G, Skov L, Thyssen JP. Association between parental autoimmune disease and atopic dermatitis in their offspring: A matched case-control study. J Eur Acad Dermatol Venereol 2019; 33(6): 1143-51.
[4]
He Z, Li X, Chen H, et al. Nobiletin attenuates lipopolysaccharide/D-galactosamine-induced liver injury in mice by activating the Nrf2 antioxidant pathway and subsequently inhibiting NF-κB-mediated cytokine production. Mol Med Rep 2016; 14(6): 5595-600.
[http://dx.doi.org/10.3892/mmr.2016.5943] [PMID: 27878238]
[5]
Weng P, Zhang XT, Sheng Q, et al. Caveolin-1 scaffolding domain peptides enhance anti-inflammatory effect of heme oxygenase-1 through interrupting its interact with caveolin-1. Oncotarget 2017; 8(25): 40104-14.
[http://dx.doi.org/10.18632/oncotarget.16676] [PMID: 28402952]
[6]
Hu X, Li L, Yan S, Li Z. Arsenic trioxide suppresses acute graftversus- host disease by activating the Nrf2/HO-1 pathway in mice. British journal of hematology 2019.
[7]
Zhao C, Jiang P, He Z, et al. Dimethyl itaconate protects against lippolysacchride-induced mastitis in mice by activating MAPKs and Nrf2 and inhibiting NF-κB signaling pathways. Microb Pathog 2019; 133103541
[http://dx.doi.org/10.1016/j.micpath.2019.05.024] [PMID: 31100405]
[8]
Chen HG, Xie KL, Han HZ, et al. Heme oxygenase-1 mediates the anti-inflammatory effect of molecular hydrogen in LPS-stimulated RAW 264.7 macrophages. Int J Surg 2013; 11(10): 1060-6.
[9]
Jiang XP, Huang XL, Yang ZP, et al. Iguratimod ameliorates inflammatory responses by modulating the Th17/Treg paradigm in dextran sulphate sodium-induced murine colitis. Mol Immunol 2018; 93: 9-19.
[http://dx.doi.org/10.1016/j.molimm.2017.10.008] [PMID: 29121519]
[10]
Viisanen T, Gazali AM, Ihantola EL, et al. FOXP3+ Regulatory T Cell compartment is altered in children with newly diagnosed Type 1 Diabetes but not in autoantibody-positive at-risk children. Front Immunol 2019; 10: 19.
[http://dx.doi.org/10.3389/fimmu.2019.00019] [PMID: 30723474]
[11]
Jiang H, Wu X, Zhu H, Xie Y, Tang S, Jiang Y. FOXP3(+)Treg/Th17 cell imbalance in lung tissues of mice with asthma. Int J Clin Exp Med 2015; 8(3): 4158-63.
[PMID: 26064325]
[12]
Gomperts E, Belcher JD, Otterbein LE, et al. The role of carbon monoxide and heme oxygenase in the prevention of sickle cell disease vaso-occlusive crises. Am J Hematol 2017; 92(6): 569-82.
[http://dx.doi.org/10.1002/ajh.24750] [PMID: 28378932]
[13]
Botto S, Gustin JK, Moses AV. The heme metabolite carbon monoxide facilitates KSHV infection by inhibiting TLR4 signaling in endothelial cells. Front Microbiol 2017; 8: 568.
[http://dx.doi.org/10.3389/fmicb.2017.00568] [PMID: 28421060]
[14]
Stocker R, Perrella MA. Heme oxygenase-1: A novel drug target for atherosclerotic diseases? Circulation 2006; 114(20): 2178-89.
[http://dx.doi.org/10.1161/CIRCULATIONAHA.105.598698] [PMID: 17101869]
[15]
Collinson EJ, Wimmer-Kleikamp S, Gerega SK, et al. The yeast homolog of heme oxygenase-1 affords cellular antioxidant protection via the transcriptional regulation of known antioxidant genes. J Biol Chem 2011; 286(3): 2205-14.
[http://dx.doi.org/10.1074/jbc.M110.187062] [PMID: 21081499]
[16]
Fall N, Barnes M, Thornton S, et al. Gene expression profiling of peripheral blood from patients with untreated new-onset systemic juvenile idiopathic arthritis reveals molecular heterogeneity that may predict macrophage activation syndrome. Arthritis Rheum 2007; 56(11): 3793-804.
[http://dx.doi.org/10.1002/art.22981] [PMID: 17968951]
[17]
Mellins ED, Macaubas C, Grom AA. Pathogenesis of systemic juvenile idiopathic arthritis: Some answers, more questions. Nat Rev Rheumatol 2011; 7(7): 416-26.
[http://dx.doi.org/10.1038/nrrheum.2011.68] [PMID: 21647204]
[18]
Gohar F, Kessel C, Lavric M, Holzinger D, Foell D. Review of biomarkers in systemic juvenile idiopathic arthritis: Helpful tools or just playing tricks? Arthritis Res Ther 2016; 18: 163.
[http://dx.doi.org/10.1186/s13075-016-1069-z] [PMID: 27411444]
[19]
van den Ham HJ, de Jager W, Bijlsma JW, Prakken BJ, de Boer RJ. Differential cytokine profiles in juvenile idiopathic arthritis subtypes revealed by cluster analysis. Rheumatology 2009; 48(8): 899-905.
[http://dx.doi.org/10.1093/rheumatology/kep125] [PMID: 19478039]
[20]
de Jager W, Hoppenreijs EP, Wulffraat NM, Wedderburn LR, Kuis W, Prakken BJ. Blood and synovial fluid cytokine signatures in patients with juvenile idiopathic arthritis: A cross-sectional study. Ann Rheum Dis 2007; 66(5): 589-98.
[http://dx.doi.org/10.1136/ard.2006.061853] [PMID: 17170049]
[21]
Mahmud SA, Binstadt BA. Autoantibodies in the pathogenesis, diagnosis, and prognosis of juvenile idiopathic arthritis. Front Immunol 2019; 9: 3168.
[http://dx.doi.org/10.3389/fimmu.2018.03168] [PMID: 30693002]
[22]
Tavakolpour S. Towards personalized medicine for patients with autoimmune diseases: Opportunities and challenges. Immunol Lett 2017; 190: 130-8.
[http://dx.doi.org/10.1016/j.imlet.2017.08.002] [PMID: 28797806]
[23]
Lei WT, Tsai PL, Chu SH, et al. Incidence and risk factors for recurrent Henoch-Schönlein purpura in children from a 16-year Nationwide database. Pediatr Rheumatol Online J 2018; 16(1): 25.
[http://dx.doi.org/10.1186/s12969-018-0247-8] [PMID: 29661187]
[24]
Shao X, Jiang C, Li Y, et al. Function of CD4(+) CD25(+) regulatory T cells in Henoch-Schonlein purpura nephritis in children. Zhonghua Er Ke Za Zhi 2014; 52(7): 516-20.
[PMID: 25224057]
[25]
Wang Q, Shi YY, Cao M, Dong W, Zhang JB. Role of imbalance between Th17 cells and Treg cells in the pathogenesis of children with Henoch-Schonlein Purpura. Zhongguo Shi Yan Xue Ye Xue Za Zhi 2015; 23(5): 1391-6.
[PMID: 26524044]
[26]
Bettelli E, Oukka M, Kuchroo VKTT. (H)-17 cells in the circle of immunity and autoimmunity. Nat Immunol 2007; 8(4): 345-50.
[http://dx.doi.org/10.1038/ni0407-345] [PMID: 17375096]
[27]
Afzali B, Lombardi G, Lechler RI, Lord GM. The role of T helper 17 (Th17) and regulatory T cells (Treg) in human organ transplantation and autoimmune disease. Clin Exp Immunol 2007; 148(1): 32-46.
[http://dx.doi.org/10.1111/j.1365-2249.2007.03356.x] [PMID: 17328715]
[28]
Giacchi V, Sciacca P, Stella I, et al. Assessment of coronary artery intimal thickening in patients with a previous diagnosis of Kawasaki disease by using high resolution transthoracic echocardiography: our experience. BMC Cardiovasc Disord 2014; 14: 106.
[http://dx.doi.org/10.1186/1471-2261-14-106] [PMID: 25139118]
[29]
Cho HJ, Yang SI, Kim KH, Kim JN, Kil HR. Cardiovascular risk factors of early atherosclerosis in school-aged children after Kawasaki disease. Korean J Pediatr 2014; 57(5): 217-21.
[http://dx.doi.org/10.3345/kjp.2014.57.5.217] [PMID: 25045363]
[30]
Straface E, Marchesi A, Gambardella L, et al. Does oxidative stress play a critical role in cardiovascular complications of Kawasaki disease? Antioxid Redox Signal 2012; 17(10): 1441-6.
[http://dx.doi.org/10.1089/ars.2012.4660] [PMID: 22578402]
[31]
Donovan EL, McCord JM, Reuland DJ, Miller BF, Hamilton KL. Phytochemical activation of Nrf2 protects human coronary artery endothelial cells against an oxidative challenge. Oxid Med Cell Longev 2012.2012132931
[http://dx.doi.org/10.1155/2012/132931] [PMID: 22685617]
[32]
Mizuno K, Toma T, Tsukiji H, et al. Selective expansion of CD16highCCR2- subpopulation of circulating monocytes with preferential production of haem oxygenase (HO)-1 in response to acute inflammation. Clin Exp Immunol 2005; 142(3): 461-70.
[http://dx.doi.org/10.1111/j.1365-2249.2005.02932.x] [PMID: 16297158]
[33]
Kelley BP, Patel SC, Marin HL, Corrigan JJ, Mitsias PD, Griffith B. Autoimmune encephalitis: Pathophysiology and imaging review of an overlooked diagnosis. AJNR Am J Neuroradiol 2017; 38(6): 1070-8.
[http://dx.doi.org/10.3174/ajnr.A5086] [PMID: 28183838]
[34]
Spatola M, Dalmau J. Seizures and risk of epilepsy in autoimmune and other inflammatory encephalitis. Curr Opin Neurol 2017; 30(3): 345-53.
[http://dx.doi.org/10.1097/WCO.0000000000000449] [PMID: 28234800]
[35]
Shen Y, Zhang ZJ, Zhu MD, Jiang BC, Yang T, Gao YJ. Exogenous induction of HO-1 alleviates vincristine-induced neuropathic pain by reducing spinal glial activation in mice. Neurobiol Dis 2015; 79: 100-10.
[http://dx.doi.org/10.1016/j.nbd.2015.04.012] [PMID: 25956228]
[36]
Lancaster E. The Diagnosis and treatment of autoimmune encephalitis. J Clin Neurol 2016; 12(1): 1-13.
[http://dx.doi.org/10.3988/jcn.2016.12.1.1] [PMID: 26754777]

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