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调节性T细胞在骨髓增生异常综合征危险分层中的研究进展

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  • 上海交通大学附属第六人民医院血液科,上海 200233

收稿日期: 2020-10-23

  网络出版日期: 2022-06-28

基金资助

国家自然科学基金(81770121)

本文引用格式

王柔嘉, 常春康 . 调节性T细胞在骨髓增生异常综合征危险分层中的研究进展[J]. 诊断学理论与实践, 2021 , 20(02) : 221 -224 . DOI: 10.16150/j.1671-2870.2021.02.019

参考文献

[1] Zeidan AM, Shallis RM, Wang R, et al. Epidemiology of myelodysplastic syndromes: why characterizing the beast is a prerequisite to taming it[J]. Blood Rev, 2019, 34:1-15.
[2] Zeidan AM, Shallis RM, Wang R, et al. Epidemiology of myelodysplastic syndromes: Why characterizing the beast is a prerequisite to taming it[J]. Blood Rev, 2019, 34:1-15.
[3] 中华医学会血液学分会. 骨髓增生异常综合征中国诊断与治疗指南(2019年版)[J]. 中华血液学杂志, 2019, 40(2):89-97.
[4] Sakaguchi S, Sakaguchi N, Asano M, et al. Immunologic self-tolerance maintained by activated T cells expressing IL-2 receptor alpha-chains (CD25). Breakdown of a single mechanism of self-tolerance causes various autoimmune diseases[J]. J Immunol, 1995, 155(3):1151-1164.
[5] Kanamori M, Nakatsukasa H, Okada M, et al. Induced regulatory T cells: their development, stability, and applications[J]. Trends Immunol, 2016, 37(11):803-811.
[6] Rueda CM, Jackson CM, Chougnet CA. Regulatory T-cell-mediated suppression of conventional T-cells and dendritic cells by different cAMP intracellular pathways[J]. Front Immunol, 2016, 7:216.
[7] Ovcinnikovs V, Ross EM, Petersone L, et al. CTLA-4-mediated transendocytosis of costimulatory molecules primarily targets migratory dendritic cells[J]. Sci Immunol, 2019, 4(35):eaaw0902.
[8] Gill H, Leung AY, Kwong YL. Molecular and cellular mechanisms of myelodysplastic syndrome: implications on targeted therapy[J]. Int J Mol Sci, 2016, 17(4):440.
[9] Korn C, Méndez-Ferrer S. Myeloid malignancies and the microenvironment[J]. Blood, 2017, 129(7):811-822.
[10] Ruggiero G, Sica M, Luciano L, et al. A case of myelodysplastic syndrome associated with CD14(+)CD56(+) monocytosis, expansion of NK lymphocytes and defect of HLA-E expression[J]. Leuk Res, 2009, 33(1):181-185.
[11] Landman S, Cruijsen M, Urbano PCM, et al. DNA methyltransferase inhibition promotes Th1 polarization in human CD4+ CD25 high FOXP3+ regulatory T cells but does not affect their suppressive capacity[J]. J Immunol Res, 2018, 2018:4973964.
[12] Leone P, Solimando AG, Malerba E, et al. Actors on the scene: immune cells in the myeloma niche[J]. Front Oncol, 2020, 10:599098.
[13] Mailloux AW, Sugimori C, Komrokji RS, et al. Expansion of effector memory regulatory T cells represents a novel prognostic factor in lower risk myelodysplastic syndrome[J]. J Immunol, 2012, 189(6):3198-208.
[14] Costantini B, Kordasti SY, Kulasekararaj AG, et al. The effects of 5-azacytidine on the function and number of regulatory T cells and T-effectors in myelodysplastic syndrome[J]. Haematologica, 2013, 98(8):1196-1205.
[15] Nishikawa H, Jäger E, Ritter G, et al. CD4+ CD25+ regulatory T cells control the induction of antigen-specific CD4+ helper T cell responses in cancer patients[J]. Blood, 2005, 106(3):1008-1011.
[16] Shi X, Zheng Y, Xu L, et al. The inflammatory cytokine profile of myelodysplastic syndromes: a meta-analysis[J]. Medicine (Baltimore), 2019, 98(22):e15844.
[17] Zou L, Barnett B, Safah H, et al. Bone marrow is a reservoir for CD4+CD25+ regulatory T cells that traffic through CXCL12/CXCR4 signals[J]. Cancer Res, 2004, 64(22):8451-8455.
[18] Fritsch RD, Shen X, Illei GG, et al. Abnormal differentia-tion of memory T cells in systemic lupus erythematosus[J]. Arthritis Rheum, 2006, 54(7):2184-2197.
[19] Kordasti SY, Ingram W, Hayden J, et al. CD4+CD25high Foxp3+ regulatory T cells in myelodysplastic syndrome (MDS)[J]. Blood, 2007, 110(3):847-850.
[20] Bleul CC, Wu L, Hoxie JA, et al. The HIV coreceptors CXCR4 and CCR5 are differentially expressed and regulated on human T lymphocytes[J]. Proc Natl Acad Sci USA, 1997, 94(5):1925-1930.
[21] Fragale A, Gabriele L, Stellacci E, et al. IFN regulatory factor-1 negatively regulates CD4+ CD25+ regulatory T cell differentiation by repressing Foxp3 expression[J]. J Immunol, 2008, 181(3):1673-1682.
[22] Pinheiro RF, Metze K, Silva MR, et al. The ambiguous role of interferon regulatory factor-1(IRF-1) immunoexpression in myelodysplastic syndrome[J]. Leuk Res, 2009, 33(10):1308-1312.
[23] Shastri A, Will B, Steidl U, et al. Stem and progenitor cell alterations in myelodysplastic syndromes[J]. Blood, 2017, 129(12):1586-1594.
[24] Wolf Y, Anderson AC, Kuchroo VK. TIM3 comes of age as an inhibitory receptor[J]. Nat Rev Immunol, 2020, 20(3):173-185.
[25] 邓圆圆, 范益民. TIM-3在肿瘤免疫中的研究进展[J]. 中华神经创伤外科电子杂志, 2016, 2(2):112-115.
[26] Sun L, Fu J, Zhou Y. Metabolism controls the balance of Th17/T-regulatory cells[J]. Front Immunol, 2017, 8:1632.
[27] Sałkowska A, Karaś K, Karwaciak I, et al. Identification of novel molecular markers of human Th17 cells[J]. Cells, 2020, 9(7):1611.
[28] Bhaskaran N, Faddoul F, Paes da Silva A, et al. IL-1β-myD88-mTOR axis promotes immune-protective IL-17A+ Foxp3+ cells during mucosal infection and is dysregula-ted with aging[J]. Front Immunol, 2020, 11:595936.
[29] Pawlik A, Anisiewicz A, Filip-Psurska B, et al. Divergent effect of tacalcitol (PRI-2191) on Th17 cells in 4T1 tumor bearing young and old ovariectomized mice[J]. Aging Dis, 2020, 11(2):241-253.
[30] Knochelmann HM, Dwyer CJ, Bailey SR, et al. When worlds collide: Th17 and Treg cells in cancer and autoimmunity[J]. Cell Mol Immunol, 2018, 15(5):458-469.
[31] Prabhala RH, Pelluru D, Fulciniti M, et al. Elevated IL-17 produced by TH17 cells promotes myeloma cell growth and inhibits immune function in multiple myeloma[J]. Blood, 2010, 115(26):5385-5392.
[32] Kahn JD, Chamuleau ME, Westers TM, et al. Regulatory T cells and progenitor B cells are independent prognostic predictors in lower risk myelodysplastic syndromes[J]. Haematologica, 2015, 100(6):e220-e222.
[33] Williamson BT, Foltz L, Leitch HA. Leitch. Autoimmune syndromes presenting as a paraneoplastic manifestation of myelodysplastic syndromes: clinical features, course, treatment and outcome hematol rep[J]. Hematol Rep, 2016, 8(2):6480.
[34] Moon HW, Kim BH, Park CM, et al. CD4+CD25high Foxp3+ regulatory T-cells in hematologic diseases[J]. Korean J Lab Med, 2011, 31(4):231-237.
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