免疫妥协与骨髓增生异常综合征

陶景莲; 韩冻; 邵宗鸿

doi:10.13201/j.issn.1004-2806.2019.11.002

免疫妥协与骨髓增生异常综合征

- 1. 天津医科大学总医院血液内科(天津, 300052);
- 2. 天津医科大学第二附属医院
基金项目:
国家自然科学基金(No:81570111、81500101、81800123)

天津市自然科学基金(No:16JCZDJC35300)

详细信息

通讯作者: 邵宗鸿,E-mail:shaozonghong@sina.com

中图分类号: R733

收稿日期: 2019-08-17

Immune compromise and myelodysplastic syndromes

More Information

Corresponding author: SHAO Zonghong, E-mail: shaozonghong@sina.com

Received Date: 17 August 2019

摘要

- 骨髓增生异常综合征 /
- 免疫妥协 /
- 免疫抑制治疗 /
- 免疫检查点分子
- myelodysplastic syndromes /
- immune compromise /
- immunosuppressive therapy /
- immune checkpoint molecule

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参考文献(40)

[1]	Li LJ,Tao JL,Fu R,et al.Increased CD34⁺CD38^-CD123⁺ cells in myelodysplastic syndrome displaying malignant features similar to those in AML[J].Int J Hematol,2014,100:60-69.
[2]	Yue LZ,Fu R,Wang HQ,et al.Expression of CD123 and CD114 on the bone marrow cells of patients with myelodysplastic syndrome[J].Chin Med J (Engl),2010,123:2034-2037.
[3]	Jiang H,Fu R,Wang H,et al.CD47 is expressed abnormally on hematopoietic cells in myelodysplastic syndrome[J].Leuk Res,2013,37:907-910.
[4]	Tao JL,Li LJ,Fu R,et al.Elevated TIM3⁺ hematopoietic stem cells in untreated myelodysplastic syndrome displayed aberrant differentiation,overproliferation and decreased apoptosis[J].Leuk Res,2014,38:714-721.
[5]	Zhang W,Shao ZH,Fu R,et al.TET2 expression in bone marrow mononuclear cells of patients with myelodysplastic syndromes and its clinical significances[J].Cancer Biol Med,2012,9:34-37.
[6]	Zhang W,Shao Z,Fu R,et al.Effect of DLK1 on tumorigenesis in CD34(+)CD38(-) bone marrow cells in myelodysplastic syndromes[J].Oncol Lett,2013,6:203-206.
[7]	Barreyro L,Will B,Bartholdy B,et al.Overexpression of IL-1 receptor accessory protein in stem and progenitor cells and outcome correlation in AML and MDS[J].Blood,2012,120:1290-1298.
[8]	Pardanani A,Finke C,Lasho TL,et al.IPSS-independent prognostic value of plasma CXCL10,IL-7 and IL-6 levels in myelodysplastic syndromes[J].Leukemia,2012,26:693-699.
[9]	Ganan-Gomez I,Wei Y,Starczynowski DT,et al.Deregulation of innate immune and inflammatory signaling in myelodysplastic syndromes[J].Leukemia,2015,29:1458-1469.
[10]	Wei Y,Dimicoli S,Bueso-Ramos C,et al.Toll-like receptor alterations in myelodysplastic syndrome[J].Leukemia,2013,27:1832-1840.
[11]	Dimicoli S,Wei Y,Bueso-Ramos C,et al.Overexpression of the toll-like receptor (TLR) signaling adaptor MYD88,but lack of genetic mutation,in myelodysplastic syndromes[J].PLoS One,2013,8:e71120.
[12]	Schneider RK,Schenone M,Ferreira MV,et al.Rps14 haploinsufficiency causes a block in erythroid differentiation mediated by S100A8 and S100A9[J].Nat Med,2016,22:288-297.
[13]	Santini V,Almeida A,Giagounidis A,et al.Randomized Phase III Study of Lenalidomide Versus Placebo in RBC Transfusion-Dependent Patients With Lower-Risk Non-del(5q) Myelodysplastic Syndromes and Ineligible for or Refractory to Erythropoiesis-Stimulating Agents[J].J Clin Oncol,2016,34:2988-2996.
[14]	Lambert C,Wu Y,Aanei C.Bone marrow immunity and myelodysplasia[J].Front Oncol,2016,6:172.
[15]	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,2012,189:3198-3208.
[16]	Hejazi M,Manser AR,Frobel J,et al.Impaired cytotoxicity associated with defective natural killer cell differentiation in myelodysplastic syndromes[J].Haematologica,2015,100:643-652.
[17]	Stringaris K,Marin D,Barrett AJ,et al.KIR gene haplotype:an independent predictor of clinical outcome in MDS patients[J].Blood,2016,128:2819-2823.
[18]	Aggarwal N,Swerdlow SH,TenEyck SP,et al.Natural killer cell (NK) subsets and NK-like T-cell populations in acute myeloid leukemias and myelodysplastic syndromes[J].Cytometry B Clin Cytom,2016,90:349-357.
[19]	Zhang W,Xie X,Mi H,et al.Abnormal populations and functions of natural killer cells in patients with myelodysplastic syndromes[J].Oncol Lett,2018,15:5497-5504.
[20]	Ma L,Ceuppens J,Kasran A,et al.Immature and mature monocyte-derived dendritic cells in myelodysplastic syndromes of subtypes refractory anemia or refractory anemia with ringed sideroblasts display an altered cytokine profile[J].Leuk Res,2007,31:1373-1382.
[21]	Zhao Z,Wang Z,Li Q,et al.The different immunoregulatory functions of mesenchymal stem cells in patients with low-risk or high-risk myelodysplastic syndromes[J].PLoS One,2012,7:e45675.
[22]	Wang Z,Tang X,Xu W,et al.The different immunoregulatory functions on dendritic cells between mesenchymal stem cells derived from bone marrow of patients with low-risk or high-risk myelodysplastic syndromes[J].PLoS One,2013,8:e57470.
[23]	Medyouf H,Mossner M,Jann JC,et al.Myelodysplastic cells in patients reprogram mesenchymal stromal cells to establish a transplantable stem cell niche disease unit[J].Cell Stem Cell,2014,14:824-837.
[24]	Chen X,Eksioglu EA,Zhou J,et al.Induction of myelodysplasia by myeloid-derived suppressor cells[J].J Clin Invest,2013,123:4595-4611.
[25]	Lechner MG,Liebertz DJ,Epstein AL.Characterization of cytokine-induced myeloid-derived suppressor cells from normal human peripheral blood mononuclear cells[J].J Immunol,2010,185:2273-2284.
[26]	Jiang HJ,Fu R,Wang HQ,et al.Increased circulating of myeloid-derived suppressor cells in myelodysplastic syndrome[J].Chin Med J (Engl),2013,126:2582-2584.
[27]	Gleason MK,Ross JA,Warlick ED,et al.CD16×CD33 bispecific killer cell engager (BiKE) activates NK cells against primary MDS and MDSC CD33+ targets[J].Blood,2014,123:3016-3026.
[28]	Ok CY,Young KH.Checkpoint inhibitors in hematological malignancies[J].J Hematol Oncol,2017,10:103.
[29]	Yang H,Bueso-Ramos C,DiNardo C,et al.Expression of PD-L1,PD-L2,PD-1 and CTLA4 in myelodysplastic syndromes is enhanced by treatment with hypomethylating agents[J].Leukemia,2014,28:1280-1288.
[30]	Haroun F,Solola SA,Nassereddine S,et al.PD-1 signaling and inhibition in AML and MDS[J].Ann Hematol,2017,96:1441-1448.
[31]	Tao J,Li L,Wang Y,et al.Increased TIM3⁺CD8⁺T cells in myelodysplastic syndrome patients displayed less perforin and granzyme B secretion and higher CD95 expression[J].Leuk Res,2016,51:49-55.
[32]	Hayashi Y,Zhang Y,Yokota A,et al.Pathobiological Pseudohypoxia as a Putative Mechanism Underlying Myelodysplastic Syndromes[J].Cancer Discov,2018,8:1438-1457.
[33]	Garcia-Manero G,Tallman MS,Martinelli G,et al.Pembrolizumab,a PD-1 Inhibitor,in Patients with Myelodysplastic Syndrome (MDS) after Failure of Hypomethylating Agent Treatment[J].Blood,2016,128:345-345.
[34]	Orskov AD,Treppendahl MB,Skovbo A,et al.Hypomethylation and up-regulation of PD-1 in T cells by azacytidine in MDS/AML patients:A rationale for combined targeting of PD-1 and DNA methylation[J].Oncotarget,2015,6:9612-9626.
[35]	Boddu P,Kantarjian H,Garcia-Manero G,et al.The emerging role of immune checkpoint based approaches in AML and MDS[J].Leuk Lymphoma,2018,59:790-802.
[36]	Jelinek T,Mihalyova J,Kascak M,et al.PD-1/PD-L1 inhibitors in haematological malignancies:update 2017[J].Immunology,2017,152:357-371.
[37]	Almeida A,Fenaux P,List AF,et al.Recent advances in the treatment of lower-risk non-del(5q) myelodysplastic syndromes (MDS)[J].Leuk Res,2017,52:50-57.
[38]	Santini V.Treatment of low-risk myelodysplastic syndromes[J].Hematology Am Soc Hematol Educ Program,2016,2016:462-469.
[39]	Fozza C.The burden of autoimmunity in myelodysplastic syndromes[J].Hematol Oncol,2018,36:15-23.
[40]	Komrokji RS,Kulasekararaj A,Al Ali NH,et al.Autoimmune diseases and myelodysplastic syndromes[J].Am J Hematol,2016,91:E280-283.