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Research Article

滤泡帮助T细胞及炎性细胞因子对重症肌无力的影响

卷 19, 期 10, 2019

页: [739 - 745] 页: 7

弟呕挨: 10.2174/1566524019666190827162615

open access plus

摘要

背景：重症肌无力（MG）是一种自身免疫性疾病，由针对骨骼肌的乙酰胆碱受体（AChR）的抗体介导。已发现各种T辅助（Th）细胞，包括Th1，Th2，Th17，Th22和滤泡辅助T（TFH）细胞的失衡与免疫功能障碍有关。 目的：本研究旨在探讨Th细胞在MG患者外周血中的作用。 材料与方法：共有33名MG患者和34名年龄匹配的对照组参加了这项研究。使用Ficoll-Paque密度梯度离心法分离外周血单个核细胞（PBMC）。通过测定细胞标志物CD4，CXCR5，CD45RO，CD45RA和ICOS和PD-1的水平，使用流式细胞术分析了PBMC中TFH细胞的比例。血清中IFN-γ，IL-4，IL-17和IL-21的水平通过细胞计数微珠阵列分析。通过ELISA分析血清IL-22水平。 结果：PBMCs中TFH细胞的频率高于健康人，并且与MG患者的严重程度相关。 MG患者血清中促炎细胞因子IFN-γ，IL-17和IL-21水平升高，而MG患者与对照组之间IL-4和IL-22水平无显着差异。 结论：我们的发现提示MG患者的Th细胞及其细胞因子平衡与MG疾病的临床状况或严重程度有关。

关键词: 重症肌无力，滤泡辅助性T细胞，T辅助性细胞，定量性重症肌无力评分，IFN-γ，IL-17。

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[1]
Mcheyzer-Williams LJ, Mcheyzer-Williams MG. Antigen-specific memory B cell development. Annu Rev Immunol 2005; 23: 487-513.
[2]
Toellner KM, Luther SA, Sze DM, et al. T helper 1 (Th1) and Th2 characteristics start to develop during T cell priming and are associated with an immediate ability to induce immunoglobulin class switching. J Exp Med 1998; 187(8): 1193-204.
[3]
Patel DD, Kuchroo VK. Th17 Cell Pathway in Human Immunity: Lessons from Genetics and Therapeutic Interventions. Immunity 2015; 43(6): 1040-51.
[4]
Xu Y, Zhu Q, Song J, et al. Regulatory Effect of Iguratimod on the Balance of Th Subsets and Inhibition of Inflammatory Cytokines in Patients with Rheumatoid Arthritis. Mediators Inflamm 2015; 2015356040
[5]
Li S, Jin T, Zhang HL, et al. Circulating Th17, Th22, and Th1 cells are elevated in the Guillain-Barre syndrome and downregulated by IVIg treatments. Mediators Inflamm 2014; 2014740947
[6]
Azizi G, Simhag A. M-M-El Rouby N, et al Th22 Cells Contribution in Immunopathogenesis of Rheumatic Diseases. Iran J Allergy Asthma Immunol 2015; 14(3): 246-54.
[7]
Schaerli P, Willimann K, Lang A, et al. Cxc chemokine receptor 5 expression defines follicular homing T cells with B cell helper function. J Exp Med 2000; 192(11): 1553-62.
[8]
Laurent C, Fazilleau N, Brousset P. A novel subset of T-helper cells: follicular T-helper cells and their markers. Haematologica 2010; 95(3): 356-8.
[9]
Simpson N, Gatenby PA, Wilson A, et al. Expansion of circulating T cells resembling follicular helper T cells is a fixed phenotype that identifies a subset of severe systemic lupus erythematosus. Arthritis Rheum 2010; 62(1): 234-44.
[10]
Zhu C, Ma J, Liu Y, et al. Increased frequency of follicular helper T cells in patients with autoimmune thyroid disease. J Clin Endocrinol Metab 2012; 97(3): 943-50.
[11]
Dai H, Sun T, Liu Z, et al. The imbalance between regulatory and IL-17-secreting CD4(+)T cells in multiple-trauma rat. Injury 2013; 44(11): 1521-7.
[12]
Wu H, Wang K, Li G, et al. Effects of transcutaneous acupoint electrical stimulation on the imbalance of Th1, Th2, Th17and Treg cells following thoracotomy of patients with lung cancer. Exp Ther Med 2016; 11(2): 495-502.
[13]
Luo C, Li Y, Liu W, et al. Expansion of circulating counterparts of follicular helper T cells in patients with myasthenia gravis. J Neuroimmunol 2013; 256(1-2): 55-61.
[14]
Schaffert H, Pelz A, Saxena A, et al. IL-17-producing CD4 T cells contribute to the loss of B-cell tolerance in experimental autoimmune myasthenia gravis. Eur J Immunol 2015.
[15]
Bossaller L, Burger J, Draeger R, et al. ICOS deficiency is associated with a severe reduction of CXCR5+CD4 germinal center Th cells. J Immunol 2006; 177(7): 4927-32.
[16]
Good-Jacobson KL, Szumilas CG, Chen L, et al. PD-1 regulates germinal center B cell survival and the formation and affinity of long-lived plasma cells. Nat Immunol 2010; 11(6): 535-42.
[17]
Nurieva RI, Chung Y, Hwang D, et al. Generation of T follicular helper cells is mediated by interleukin-21 but independent of T helper 1, 2, or 17 cell lineages. Immunity 2008; 29(1): 138-49.
[18]
Ettinger R, Sims GP, Fairhurst AM, et al. IL-21 Induces Differentiation of Human Naive and Memory B Cells into Antibody-Secreting Plasma Cells. The Journal of Immunology, 2005; 175(12): 7867-79.
[19]
Trowbridge IS, Thomas ML. CD45: an emerging role as a protein tyrosine phosphatase required for lymphocyte activation and development. Annual Review of Immunology 1994; 12(1): 85.
[20]
Kung C, Pingel JT, Heikinheimo M, et al. Mutations in the tyrosine phosphatase CD45 gene in a child with severe combined immunodeficiency disease. Nat Med 2000; 6(3): 343-5.
[21]
Huang S, Wang W, Chi L. Feasibility of up-regulating CD4+CD25+ Tregs by IFN-γ in myasthenia gravis patients. BMC Neurol 2015; 15(1): 1-10.
[22]
Curtis JR, Westfall AO, Allison J, et al. Population-based assessment of adverse events associated with long-term glucocorticoid use. Arthritis Rheum 2006; 55(3): 420-6.
[23]
Bai Y, Liu R, Huang D, et al. CCL2 recruitment of IL-6-producing CD11b+ monocytes to the draining lymph nodes during the initiation of Th17-dependent B cell-mediated autoimmunity. Eur J Immunol 2008; 38: 1877-88.
[24]
Cheng F, Guo Z, Xu H, et al. Decreased plasma IL22 levels, but not increased IL17 and IL23 levels, correlate with disease activity in patients with systemic lupus erythematosus. Ann Rheum Dis 2009; 68(4): 604-6.

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