髓源抑制性細(xì)胞在非腫瘤疾病中的研究進(jìn)展

喻蓉，于化鵬

·綜 述·

髓源抑制性細(xì)胞在非腫瘤疾病中的研究進(jìn)展

喻蓉，于化鵬

髓源抑制性細(xì)胞(MDSCs)是一群在病理?xiàng)l件下產(chǎn)生的具有明顯抑制功能的天然免疫細(xì)胞，可通過(guò)不同機(jī)制對(duì)多種免疫細(xì)胞產(chǎn)生抑制作用，從而導(dǎo)致機(jī)體先天性和獲得性免疫功能低下，促進(jìn)疾病的發(fā)展及惡化。對(duì)MDSCs的研究最早集中在腫瘤領(lǐng)域，近年來(lái)關(guān)于其在非腫瘤疾病中的研究日益增多，現(xiàn)就其在非腫瘤疾病的研究進(jìn)展作一綜述。

髓源抑制性細(xì)胞；非腫瘤疾?。幻庖哒{(diào)節(jié)

1 髓源抑制性細(xì)胞(MDSCs)概述

1984年Hertel-Wulff研究小組在腫瘤組織中發(fā)現(xiàn)一群具有抑制先天或獲得性免疫反應(yīng)作用的細(xì)胞，這群細(xì)胞主要由不成熟的巨噬細(xì)胞、粒細(xì)胞、髓樣樹突細(xì)胞等髓系細(xì)胞組成，故將它們命名為髓源抑制性細(xì)胞(myeloid-derived suppressor cells，MDSCs)[1]。

1.1 MDSCs的產(chǎn)生與調(diào)節(jié) MDSCs屬于骨髓造血干細(xì)胞，該類細(xì)胞可產(chǎn)生無(wú)抑制功能的未成熟髓樣細(xì)胞(immature myeloid cells，IMCs)[2]。在正常情況下，IMCs可遷移至外周淋巴器官，并分化為成熟的樹突細(xì)胞、巨噬細(xì)胞和(或)粒細(xì)胞。在病理?xiàng)l件下(如腫瘤、炎癥、外傷、移植手術(shù)及自身免疫性疾病等)，IMCs分化為正?？乖蔬f細(xì)胞的能力下降，聚集在外周病理組織及淋巴器官中，逐漸顯示出免疫抑制功能，成為MDSCs[3-4]。因此，在健康人的肝臟和脾臟中，MDSCs所占比例不到5%，從外周血單核細(xì)胞中分離到的MDSCs占所有細(xì)胞的比例不到1%[2]。

小鼠MDSCs的主要表面標(biāo)記物是CD11b和Gr-1，后者包括Ly6G和Ly6C[5]，據(jù)此有學(xué)者將MDSCs分為CD11b+Ly6ClowLy6G+中性粒細(xì)胞和CD11b+Ly6ChighLy6G－單核細(xì)胞兩種亞型[6]，后續(xù)又有學(xué)者報(bào)道了CD11b+Ly6C－Ly6G+、CD11b+Ly6CLy6G－、CD11b+Ly6C+Ly6G－、CD11b+Ly6C+Ly6G+等多種亞型[7-9]，各亞型的產(chǎn)生時(shí)間、功能、代謝產(chǎn)物及在腫瘤中的分布均有所不同。某些小鼠的MDSCs還表達(dá)IL-4Rα、F4/80、CD115、CD80等表面標(biāo)記分子[10-14]。在腫瘤患者中，MDSCs的主要標(biāo)志為CD11b+、CD33+、CD34+、CD14－HLA-DR－以及CD15[15-18]。新近在黑色素瘤和肝癌患者體內(nèi)還發(fā)現(xiàn)了表面標(biāo)志為CD14+HLA-DR－/low的細(xì)胞群，提示不同的腫瘤可產(chǎn)生不同的MDSCs細(xì)胞亞群[15,19]。

MDSCs的調(diào)節(jié)受多種細(xì)胞因子的影響，這些細(xì)胞因子主要可以概括為兩大類。第一類由腫瘤細(xì)胞產(chǎn)生，可促進(jìn)MDSCs擴(kuò)增，如環(huán)氧合酶2、前列腺素、干細(xì)胞因子、巨噬細(xì)胞集落刺激因子、粒巨噬細(xì)胞集落刺激因子、白細(xì)胞介素6(interleukin-6，IL-6)、血管內(nèi)皮生長(zhǎng)因子等[20-24]，它們主要通過(guò)激活蛋白酪氨酸激酶途徑(JAK)和信號(hào)轉(zhuǎn)導(dǎo)與轉(zhuǎn)錄激活途徑3(STAT3)促進(jìn)MDSCs擴(kuò)增[25]。第二類是由活化的T細(xì)胞和腫瘤基質(zhì)產(chǎn)生，直接參與MDSCs的活化[26]。該類細(xì)胞因子包括γ干擾素、Toll樣受體、IL-13、IL-4、轉(zhuǎn)化生長(zhǎng)因子β等，它們主要通過(guò)STAT1、SAT6和核因子NF-κB途徑促進(jìn)MDSCs的活化[27]。

1.2 MDSCs的免疫抑制機(jī)制 MDSCs主要通過(guò)其表面受體和(或)釋放的可溶性介質(zhì)發(fā)揮免疫抑制作用，如精氨酸(Arginine，Arg)、誘導(dǎo)型一氧化氮合酶(inducible nitric oxide synthases，iNOS)、活性氧族(reactive oxygen species，ROS)、過(guò)亞硝酸鹽等。Arg通過(guò)減少表達(dá)CD3ζ[28]和阻止細(xì)胞周期蛋白D3以及細(xì)胞周期依耐性蛋白激酶4而阻止T細(xì)胞增殖[29]。iNOS通過(guò)阻斷JAK3和STAT5轉(zhuǎn)錄激活途徑[30]，阻止主要組織相容性復(fù)合物Ⅱ(major histocompatibility complex，MHCⅡ)的表達(dá)[31]，從而抑制T細(xì)胞功能。ROS和過(guò)亞硝酸鹽則通過(guò)催化T細(xì)胞受體硝化抑制CD8+T細(xì)胞，阻斷T細(xì)胞與MHC的交互作用[32]。另有研究表明，不同亞型MDSCs抑制T細(xì)胞的機(jī)制不同，如粒細(xì)胞型MDSCs高表達(dá)ROS、低表達(dá)NO，單核細(xì)胞型MDSCs卻與之相反，但是這兩種亞型都表達(dá)Arg1[33]。Movahedi等[6]也發(fā)現(xiàn)在荷瘤小鼠中，這兩種亞型的細(xì)胞對(duì)特異性T細(xì)胞抗原的抑制機(jī)制不同，粒細(xì)胞型主要通過(guò)Arg1途徑，而單核細(xì)胞型則通過(guò)STAT1和iNOS途徑抑制T細(xì)胞增殖。

2 MDSCs在非腫瘤疾病中的研究進(jìn)展

MDSCs最初是在腫瘤組織中被發(fā)現(xiàn)的，所以目前其研究重點(diǎn)也集中在腫瘤領(lǐng)域。但近年來(lái)也有不少學(xué)者將其特有的免疫抑制作用運(yùn)用于非腫瘤疾病中。

2.1 急性感染 一些實(shí)驗(yàn)證明MDSCs在急慢性感染中數(shù)量增多，如急性肝炎時(shí)，體內(nèi)的免疫系統(tǒng)被激活，機(jī)體通過(guò)各種免疫細(xì)胞和因子對(duì)病原體進(jìn)行清除。但是，過(guò)強(qiáng)的免疫反應(yīng)對(duì)自身的組織和細(xì)胞反而會(huì)起到破壞作用。小鼠急性肝炎模型中，肝臟特異性糖蛋白130(glycoprotein，gp130)的缺失可導(dǎo)致病死率顯著增加，而gp130可以通過(guò)gp130-STAT途徑誘導(dǎo)MDSCs增殖[34]。急性肝炎時(shí)，通過(guò)輔助性T細(xì)胞分泌γ干擾素調(diào)節(jié)作用，可誘導(dǎo)MDSCs的增殖，因此，MDSCs可能對(duì)肝臟起到保護(hù)作用。但在肝癌患者體內(nèi)MDSCs的數(shù)量也是增多的[35]，推測(cè)可能是MDSCs對(duì)急性期肝炎有免疫保護(hù)作用，而后期則參與肝纖維化形成和肝癌的進(jìn)展，但具體機(jī)制仍有待研究證實(shí)。在脊髓急性損傷患者的外周血標(biāo)本中，CD11b+Ly6C+Ly6G－亞型MDSCs明顯增多，這些細(xì)胞通過(guò)上調(diào)iNOS和Arg1的表達(dá)對(duì)T細(xì)胞發(fā)揮抑制作用，有利于血管生長(zhǎng)，加速去除脊髓損傷后的血腫，并有抗炎作用[9]。

2.2 移植免疫 先天固有免疫在啟動(dòng)同種移植排斥反應(yīng)和移植物存活中發(fā)揮著非常重要的作用。MDSCs通過(guò)與細(xì)胞接觸并分泌大量iNOS抑制移植物內(nèi)T細(xì)胞活化并誘導(dǎo)T細(xì)胞凋亡，抑制移植反應(yīng)，對(duì)宿主起到保護(hù)作用。例如在同種異基因腎移植模型中，抗CD28抗體可誘導(dǎo)移植物和外周血中MDSCs擴(kuò)增，使體內(nèi)iNOS水平升高，從而建立免疫耐受，若抑制iNOS活性，可打破已建立的免疫耐受[36]。肝星狀細(xì)胞中可溶性因子介導(dǎo)的γ干擾素信號(hào)途徑可誘導(dǎo)MDSCs增殖，在同種異體肝臟移植中能促使宿主體內(nèi)CD8+T細(xì)胞凋亡和輔助性T細(xì)胞增殖，促發(fā)免疫抑制，從而使宿主獲得長(zhǎng)期存活[37]。另有研究發(fā)現(xiàn)，接受粒細(xì)胞集落刺激因子(G-CSF)治療的干細(xì)胞移植患者，外周血中MDSCs數(shù)量顯著增加，在體外將這群細(xì)胞與T淋巴細(xì)胞共培養(yǎng)后可發(fā)現(xiàn)其抑制了T淋巴細(xì)胞反應(yīng)[38]。

2.3 支氣管哮喘/哮喘 哮喘的發(fā)病機(jī)制復(fù)雜，普遍認(rèn)為Th1/Th2失衡在哮喘的發(fā)病機(jī)制中發(fā)揮了重要作用。但是，新近有研究認(rèn)為哮喘患者對(duì)過(guò)敏原存在免疫耐受機(jī)制缺陷是導(dǎo)致Th1/Th2失衡的重要原因[39]，過(guò)強(qiáng)的先天性免疫和獲得性免疫均可促進(jìn)哮喘氣道炎癥[40]。研究表明，脂多糖誘導(dǎo)的MDSCs可上調(diào)特異性轉(zhuǎn)錄因子核心堿基序列3或誘導(dǎo)已接觸抗原的Th2細(xì)胞STAT5活化，使樹突細(xì)胞促進(jìn)Th2細(xì)胞因子產(chǎn)生的能力受到抑制，Th2細(xì)胞激活被抑制，氣道炎癥得到緩解[41]。MDSCs還能通過(guò)上調(diào)CD4+CD25+Foxp3+Treg細(xì)胞的數(shù)量，抑制嗜酸性粒細(xì)胞的產(chǎn)生，從而減輕氣道炎癥[42]。另有研究發(fā)現(xiàn)，不同亞型的MDSCs對(duì)哮喘氣道炎癥的作用不同，其中CD11b+Ly6C+Ly6G－可下調(diào)T細(xì)胞活性，募集Treg細(xì)胞，減輕氣道高反應(yīng)性；CD11b+Ly6CLy6G+則與之相反，具有促炎作用，可加重氣道高反應(yīng)性[8]。小部分CD11b+Ly6C+Ly6G+亞型通過(guò)Arg代謝途徑也可抑制T細(xì)胞反應(yīng)[43]。

3 展望

因MDSCs在病理?xiàng)l件下具有特殊的免疫調(diào)控作用，其調(diào)控及臨床應(yīng)用已成為目前的研究熱點(diǎn)。針對(duì)MDSCs治療的初步成功，為腫瘤及非腫瘤疾病的治療提供了新的思路和方向。但是利用其治療非腫瘤疾病仍有許多未知的情況亟待進(jìn)一步闡明。首先，MDSCs最先在腫瘤疾病中發(fā)現(xiàn)，可促進(jìn)腫瘤細(xì)胞生長(zhǎng)，利用其治療非腫瘤疾病是否會(huì)導(dǎo)致腫瘤發(fā)生？其次，MDSCs的具體免疫機(jī)制及其與其他免疫因子的關(guān)系目前仍未完全闡明；第三，MDSCs眾多亞型的作用各不相同，如何才能利用其各自優(yōu)點(diǎn)發(fā)揮治療作用？第四，MDSCs是如何從骨髓遷移至脾臟、外周血、淋巴細(xì)胞和病理組織的？局部組織在病理情況下是否也會(huì)產(chǎn)生MDSCs？第五，過(guò)繼轉(zhuǎn)移MDSCs細(xì)胞治療一些非腫瘤疾病初見成效，但哪種過(guò)繼轉(zhuǎn)移方式才能使MDSCs細(xì)胞直接聚集于治療的靶器官仍不明確；第六，誘導(dǎo)自身產(chǎn)生與體外過(guò)繼相比，哪種方法的治療效果更好，如何才能在體外獲得臨床可用、數(shù)量足夠的MDSCs，目前仍是一個(gè)難題。這些問(wèn)題的解決，對(duì)MDSCs在非腫瘤疾病中的應(yīng)用和相關(guān)機(jī)制的闡釋以及在臨床上的應(yīng)用將產(chǎn)生重要促進(jìn)作用。

[1] Hertel-Wulff B, Okada S, Oseroff A,et al.In vitropropagation and cloning of murine natural suppressor (NS) cells[J]. J Immunol, 1984, 133(5): 2791-2796.

[2] Gabrilovich DI, Nagaraj S. Myeloid-derived suppressor cells as regulators of the immune system[J]. Nat Rev Immunol, 2009, 9(3): 162-174.

[3] Gabrilovich D. Mechanisms and functional significance of tumour-induced dendritic-cell defects[J]. Nat Rev Immunol, 2004, 4(12): 941-952.

[4] Cui ZY, Huang YT, Zhao JM,et al. Dynamic observation with the method of cytometry on the dendritic cell-induced proliferation profile of T cells[J]. J Zhengzhou Univ (Med Sci), 2005, 40(9): 822-824.[崔自由, 黃幼田, 趙繼敏, 等. 應(yīng)用流式細(xì)胞術(shù)動(dòng)態(tài)觀測(cè)小鼠樹突狀細(xì)胞誘導(dǎo)的T細(xì)胞增殖的變化[J]. 鄭州大學(xué)學(xué)報(bào)(醫(yī)學(xué)版), 2005, 40(9): 822-824.]

[5] Ostrand-Rosenberg S, Sinha P. Myeloid-derived suppressor cells: linking inflammation and cancer[J]. J Immunol, 2009, 182(8): 4499-4506.

[6] Movahedi K, Guilliams M, Van den Bossche J,et al. Identification of discrete tumor-induced myeloid-derived suppressor cell subpopulations with distinct T cell-suppressive activity[J]. Blood, 2008, 111(8): 4233-4244.

[7] Peranzoni E, Zilio S, Marigo I,et al. Myeloid-derived suppressor cell heterogeneity and subset definition[J]. Curr Opin Immunol, 2010, 22(2): 238-244.

[8] Deshane J, Zmijewski JW, Luther R,et al. Free radicalproducing myeloid-derived regulatory cells: potent activators and suppressors of lung inflammation and airway hyperresponsiveness[J]. Mucosal Immunol, 2011, 4(5): 503-518.

[9] Saiwai H, Kumamaru H, Ohkawa Y,et al. Ly6C+Ly6G–myeloidderived suppressor cells play a critical role in the resolution of acute inflammation and the subsequent tissue repair process after spinal cord injury[J]. J Neurochem, 2013, 125(1): 74-88.

[10] Gallina G, Dolcetti L, Serafini P,et al. Tumors induce a subset of inflammatory monocytes with immunosuppressive activity on CD8+ T cells[J]. J Clin Invest, 2006, 116(10): 2777-2790.

[11] Umemura N, Saio M, Suwa T,et al. Tumor-infiltrating myeloidderived suppressor cells are pleiotropic-inflamed monocytes/ macrophages that bear M1- and M2-type characteristics[J]. J Leukoc Biol, 2008, 83(5): 1136-1144.

[12] Rossner S, Voigtlander C, Wiethe C,et al. Myeloid dendritic cell precursors generated from bone marrow suppress T cell responsesviacell contact and nitric oxide productionin vitro[J]. Eur J Immunol, 2005, 35(12): 3533-3544.

[13] Huang B, Pan PY, Li Q,et al. Gr-1+CD115+immature myeloid suppressor cells mediate the development of tumor-induced T regulatory cells and T-cell anergy in tumor-bearing host[J]. Cancer Res, 2006, 66(2): 1123-1131.

[14] Yang R, Cai Z, Zhang Y,et al. CD80 in immune suppression by mouse ovarian carcinoma-associated Gr-1+CD11b+ myeloid cells[J]. Cancer Res, 2006, 66(13): 6807-6815.

[15] Filipazzi P, Valenti R, Huber V,et al. Identification of a new subset of myeloid suppressor cells in peripheral blood of melanoma patients with modulation by a granulocytemacrophage colony-stimulation factor-based antitumor vaccine[J]. J Clin Oncol, 2007, 25(18): 2546-2553.

[16] Zea AH, Rodriguez PC, Atkins MB,et al. Arginase-producing myeloid suppressor cells in renal cell carcinoma patients: a mechanism of tumor evasion[J]. Cancer Res, 2005, 65(8): 3044-3048.

[17] Mirza N, Fishman M, Fricke I,et al. All-trans-retinoic acid improves differentiation of myeloid cells and immune response in cancer patients[J]. Cancer Res, 2006, 66(18): 9299-9307.

[18] Srivastava MK, Bosch JJ, Thompson JA,et al. Lung cancer patients' CD4+T cells are activatedin vitroby MHC Ⅱ cellbased vaccines despite the presence of myeloid-derived suppressor cells[J]. Cancer Immunol Immunother, 2008, 57(10): 1493-1504.

[19] Hoechst B, Ormandy LA, Ballmaier M,et al. A new population of myeloid-derived suppressor cells in hepatocellular carcinoma patients induces CD4+CD25+Foxp3+T cells[J]. Gastroenterology, 2008, 135(1): 234-243.

[20] Pan PY, Wang GX, Yin B,et al. Reversion of immune tolerance in advanced malignancy: modulation of myeloid-derived suppressor cell development by blockade of stem-cell factor function[J]. Blood, 2008, 111(1): 219-228.

[21] Sinha P, Clements VK, Fulton AM,et al. Prostaglandin E2 promotes tumor progression by inducing myeloid-derived suppressor cells[J]. Cancer Res, 2007, 67(9): 4507-4513.

[22] Serafini P, Carbley R, Noonan KA,et al. High-dose granulocytemacrophage colony-stimulating factor-producing vaccines impair the immune response through the recruitment of myeloid suppressor cells[J]. Cancer Res, 2004, 64(17): 6337-6343.

[23] Bunt SK, Yang L, Sinha P,et al. Reduced inflammation in the tumor microenvironment delays the accumulation of myeloidderived suppressor cells and limits tumor progression[J]. Cancer Res, 2007, 67(20): 10019-10026.

[24] Gabrilovich D, Ishida T, Oyama T,et al. Vascular endothelial growth factor inhibits the development of dendritic cells and dramatically affects the differentiation of multiple hematopoietic lineagesin vivo[J]. Blood, 1998, 92(11): 4150-4166.

[25] Bromberg J. Stat proteins and oncogenesis[J]. J Clin Invest,2002, 109(9): 1139-1142.

[26] Delano MJ, Scumpia PO, Weinstein JS,et al. MyD88-dependent expansion of an immature GR-1+CD11b+population induces T cell suppression and Th2 polarization in sepsis[J]. J Exp Med, 2007, 204(6): 1463-1474.

[27] Gabrilovich DI, Nagaraj S. Myeloid-derived suppressor cells as regulators of the immune system[J]. Nat Rev Immunol, 2009, 9(3): 162-174.

[28] Rodriguez PC, Zea AH, Culotta KS,et al. Regulation of T cell receptor CD3zeta chain expression by L-arginine[J]. J Biol Chem, 2002, 277(24): 21123-21129.

[29] Rodriguez PC, Quiceno DG, Ochoa AC. L-arginine availability regulates T-lymphocyte cell-cycle progression[J]. Blood, 2007, 109(4): 1568-1573.

[30] Bingisser RM, Tilbrook PA, Holt PG,et al. Macrophage-derived nitric oxide regulates T cell activationviareversible disruption of the Jak3/STAT5 signaling pathway[J]. J Immunol, 1998, 160(12): 5729-5734.

[31] Harari O, Liao JK. Inhibition of MHC II gene transcription by nitric oxide and antioxidants[J]. Curr Pharm Des, 2004, 10(8): 893-898.

[32] Nagaraj S, Gupta K, Pisarev V,et al. Altered recognition of antigen is a mechanism of CD8+ T cell tolerance in cancer[J]. Nat Med, 2007, 13(7): 828-835.

[33] Youn JI, Park SH, Jin HT,et al. Enhanced delivery efficiency of recombinant adenovirus into tumor and mesenchymal stem cells by a novel PTD[J]. Cancer Gene Ther, 2008, 15(11): 703-712.

[34] Sander LE, Sackett SD, Dierssen U,et al. Hepatic acute-phase proteins control innate immune responses during infection by promoting myeloid-derived suppressor cell function[J]. J Exp Med, 2010, 207(7): 1453-1464.

[35] Cripps JG, Wang J, Maria A,et al. Type 1 T helper cells induce the accumulation of myeloid-derived suppressor cells in the inflamed Tgfb1 knockout mouse liver[J]. Hepatology, 2010, 52(4): 1350-1359.

[36] Dugast AS, Haudebourg T, Coulon F,et al. Myeloid-derived suppressor cells accumulate in kidney allograft tolerance and specifically suppress effector T cell expansion[J]. J Immunol, 2008, 180(12): 7898-7906.

[37] Chou HS, Hsieh CC, Yang HR,et al. Hepatic stellate cells regulate immune response by way of induction of myeloid suppressor cells in mice[J]. Hepatology, 2011, 53(3): 1007-1019.

[38] Luyckx A, Schouppe E, Rutgeerts O,et al. G-CSF stem cell mobilization in human donors induces polymorphonuclear and mononuclear myeloid-derived suppressor cells[J]. Clin Immunol, 2012, 143(1): 83-87.

[39] Ma JJ, Lu N, Chen BL,et al. Regulatory effects of transcription factor RORγt on the balance of Th17/Treg in asthma model in pregnant mouse[J]. Med J Chin PLA, 2012, 37(6): 561-568.[馬佳佳, Nick Lu, 陳必良, 等. 轉(zhuǎn)錄因子RORγt對(duì)妊娠期哮喘模型小鼠Th17/Treg平衡的調(diào)節(jié)作用[J]. 解放軍醫(yī)學(xué)雜志, 2012, 37(6): 561-568.]

[40] Eisenbarth SC, Cassel S, Bottomly K. Understanding asthma pathogenesis: linking innate and adaptive immunity[J]. Curr Opin Pediatr, 2004, 16(6): 659-666.

[41] Arora M, Poe SL, Oriss TB,et al. TLR4/MyD88-induced CD11b+Gr-1 int F4/80+ non-migratory myeloid cells suppress Th2 effector function in the lung[J]. Mucosal Immunol, 2010, 3(6): 578-593.

[42] Zheng YN, Yu HP, Chen X,et al. Effect and mechanism of lipopolysaccharides-induced myeloid-derived suppressor on airway inflammation in asthmatic mice[J]. Natl Med J Chin, 2012, 92(44): 3147-3150. [鄭燕妮, 于化鵬, 陳新, 等. 脂多糖誘導(dǎo)髓源抑制性細(xì)胞對(duì)哮喘小鼠氣道炎癥的影響及其機(jī)制[J]. 中華醫(yī)學(xué)雜志, 2012, 92(44): 3147-3150.]

[43] Rodriguez PC, Ernstoff MS, Hernandez C,et al. Arginase I-producing myeloid-derived suppressor cells in renal cell carcinoma are a subpopulation of activated granulocytes[J]. Cancer Res, 2009, 69(4): 1553-1560.

Advance in researches on myeloid-derived suppressor cells in non-neoplastic diseases

YU Rong, YU Hua-peng*
Department of Respiratory Diseases, Zhujiang Hospital, Southern Medical University, Guangzhou 510282, China
*

, E-mail: huapengyu@yahoo.com.cn

Myeloid-derived suppressor cells (MDSCs) are a population of innate immune cells that form under pathological conditions, possess outstanding inhibitory function, and exert immune inhibitory function on many kinds of immune cells by different mechanisms, thus resulting in suppression of innate immune function and acquired immune function, and then promoting progression and deterioration of disease. The earliest researches about MDSCs focused on oncology field. In recent years, the researches about immune inhibition of MSCs in non-neoplastic diseases is increasing. The present paper reviews the research progresses of MDSCs in non-neoplastic diseases.

myeloid derived suppressor cells; non-neoplastic diseases; immunomodulatory

R392.3

A

0577-7402(2013)10-0864-04

10.11855/j.issn.0577-7402.2013.10.018

2013-04-12；

2013-07-17)

(責(zé)任編輯：沈?qū)?

喻蓉，碩士研究生。主要從事哮喘機(jī)制方面的研究

510282 廣州 南方醫(yī)科大學(xué)珠江醫(yī)院呼吸內(nèi)科(喻蓉、于化鵬)

于化鵬，E-mail: huapengyu@yahoo.com.cn