幽门螺杆菌(Hp)感染可诱导强烈的先天性免疫和特异性免疫应答。然而,如果未经治疗,Hp感染不会消失,慢性活动性胃炎将会持续进展。胃炎的局部状态及其免疫应答是细菌持续存在的主要原因和最终的临床结果 。调节性T细胞在Hp感染中作用已经有许多争议,它可抑制机体对Hp的免疫应答,从而减轻急性炎症的发生,但同时也造成Hp在胃黏膜中的长期定植,从而使慢性感染持续存在,导致病变的进一步发展。现将调节性T细胞在Hp感染的不同临床表现中的作用作一综述。
Abstract
Helicobacter pylori (H.pylori) colonization can induce vigorously innate and specific immune responses.However,the infection will not disappear and chronic active gastritis will continue if left untreated.It has been established that the topographical pattern of gastritis and its immune response are the main causes for the persistence of bacteria and the clinical outcome.There have been many controversies over the role of Treg cells in H.pylori infection.Treg cells can inhibit the body's immune response to Hp,thereby reducing the incidence of acute inflammation.At the same time,the response inhibition also causes long-term colonization of Hp in gastric mucosa and the persistence of chronic infection,leading to the further development of the disease.This paper reviews the role of Treg in different clinical expressions of H.Pylori infection.
关键词
幽门螺杆菌 /
调节性T细胞 /
儿童 /
胃癌
Key words
Helicobacter pylor /
regulatory T-cell /
children /
gastric cancer
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参考文献
[1] Bagheri N,Azadegan-Dehkordi F,Rahimian G,et al.Altered Th17 cytokine expression in helicobacter pylori patients with TLR4 (D299G) Polymorphism[J].Immunol Invest,2016,45(2):161-171.
[2] Miftahussurur M,Yamaoka Y.Helicobacter pylori virulence genes and host genetic polymorphisms as risk factors for peptic ulcer disease[J].Expert Rev Gastroent,2015,9(12):1535-1547.
[3] Bagheri N,Azadegan-Dehkordi F,Shirzad M,et al.Mucosal interleukin-21 mRNA expression level is high in patients with Helicobacter pylori and is associated with the severity of gastritis[J].Cent Eur J Immunol,2015,40:61-67.
[4] Salimzadeh L,Bagheri N,Zamanzad B,et al.Frequency of virulence factors in Helicobacter pylori-infected patients with gastritis[J].Microb Pathog,2015,80:67-72.
[5] Rahimian G,Sanei MH,Shirzad H,et al.Virulence factors of Helicobacter pylori vacA increase markedly gastric mucosal TGF-β1 mRNA expression in gastritis patients[J].Microb Pathog,2014,67:1-7.
[6] Thi Huyen Trang T,Thanh Binh T,Yamaoka Y.Relationship between vacA types and development of gastroduodenal diseases[J].Toxins,2016,8(6):182.
[7] Müller A,Oertli M,Arnold IC.H.pylori exploits and manipulates innate and adaptive immune cell signaling pathways to establish persistent infection[J].Cell Commun Signal,2011,9(1):1.
[8] Raju D,Hussey S,Ang M,et al.Vacuolating cytotoxin and variants in Atg16L1 that disrupt autophagy promote Helicobacter pylori infection in humans[J].Gastroenterology,2012,142(5):1160-1171.
[9] Hashempour T,Bamdad T,Bergamini A,et al.F protein increases CD4+ CD25+ T cell population in patients with chronic hepatitis C[J].Pathogens and Disease,2015,73(4):ftv022.
[10] Shevach EM.Mechanisms of foxp3+ T regulatory cell-mediated suppression[J].Immunity,2009,30(5):636-645.
[11] Miyara M,Yoshioka Y,Kitoh A,et al.Functional delineation and differentiation dynamics of human CD4+ T cells expressing the FoxP3 transcription factor[J].Immunity,2009,30(6):899-911. [12] Noack M,Miossec P.Th17 and regulatory T cell balance in autoimmune and inflammatory diseases[J].Autoimmu Rev,2014,13(6):668-677.
[13] Enk AH.Dendritic cells in tolerance induction[J].Immunol Lett,2005,99(1):8-11.
[14] Collison LW,Workman CJ,Kuo TT,et al.The inhibitory cytokine IL-35 contributes to regulatory T-cell function[J].Nature,2007,450(7169):566-569.
[15] Larussa T,Leone I,Suraci E,et al.Helicobacter pylori and T helper cells:Mechanisms of immune escape and tolerance[J].J Immunol Res,2015,2015.
[16] Kao JY,Zhang M,Miller MJ,et al.Helicobacter pylori immune escape is mediated by dendritic cell–induced Treg skewing and Th17 suppression in mice[J].Gastroenterology,2010,138(3):1046-1054.
[17] Serrano C,Wright SW,Bimczok D,et al.Downregulated Th17 responses are associated with reduced gastritis in Helicobacter pylori-infected children[J].Mucosal Immunol,2013,6(5):950-959.
[18] Robinson K,Kenefeck R,Pidgeon EL,et al.Helicobacter pylori- induced peptic ulcer disease is associated with inadequate regulatory T cell responses[J].Gut,2008,57(10):1375-1385.
[19] Kindlund B,Sjöling Å,Hansson M,et al.FOXP3-expressing CD4+ T-cell numbers increase in areas of duodenal gastric metaplasia and are associated to CD4+ T-cell aggregates in the duodenum of helicobacter pylori-infected duodenal ulcer patients[J].Helicobacter,2009,14(3):192-201.
[20] Jang TJ.The number of Foxp3-positive regulatory T cells is increased in Helicobacter pylori gastritis and gastric cancer[J].Pathol Res Pract,2010,206(1):34-38.
[21] García M,Bellosillo B,Sanchez-Gonzalez B,et al.Study of regulatory T-cells in patients with gastric malt lymphoma:influence on treatment response and outcome[J].PLoS One,2012,7(12):e51681.
[22] Iwaya Y,Kobayashi M,Momose M,et al.High levels of FOXP3+ regulatory T cells in gastric MALT lymphoma predict responsiveness to Helicobacter pylori eradication[J].Helicobacter,2013,18(5):356-362.
[23] Amedei A,Codolo G,Del Prete G,et al.The effect of Helicobacter pylori on asthma and allergy[J].J Asthma Allergy,2010,3:139-147.
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