老年CD+7急性髓系白血病生物学特征及其临床意义

目的 研究老年CD7抗原阳性急性髓性白血病（CD^＋7AML）的临床生物学特征。方法 对98便初治老年AML进行细胞形态学、免疫表型、多药耐药P糖蛋白（P120）、细胞遗传学核型分析，并采用常规AML方案诱导治疗，判定疗效。结果 老年AML中CD7阳性表达率28.57%（28/98）,28例CD^＋7老年AML（M/F，20/8）的FAB分型结果为：M03例、M13例、M2a6例、M4a2例、M4b1例、M5a1例、M5b9例。CD^＋7老年AML患者外周血白细胞计数（53.80 vs 25.21 P=0.001）、原始细胞比例（69.00% vs 41.02% P=0.001）及P-糖蛋白表达显著增高（67.85 vs 28.57 P=0.001）,肝脏肿大（46.10% vs 23.50% P=0.044）和髓外白血病易发（28.57% vs 2.78% P=0.001）,且对常规化疗反应差，预后不良，完全缓解率亚型，常提示预后不良，建议监测初诊AML患者CD7表达。     

白血病细胞共刺激分子和MHC分子的表达分析

目的：检测各型白血病细胞表面共刺激分子和MHC分子的表达情况。方法：采集66例初诊白血病患者骨髓标本细胞及15例正常人外周血标本，分离单个核细胞，采用直接荧光抗体标记，应用流式细胞仪检测细胞表面CD80（B7—1）、CD86（B7—2）、HLA-DR和HLA-ABC的表达。结果：所有66白血病患者，仅1例急性髓细胞白血病（AML）与1例B-ALL表达CDS0，其余均为CD80阴性表达;CD88在急性淋巴细胞白血病（ALL）及慢性髓细胞白血病（CML）组的表达低于健康对照；HLA-DR的表达仅在CML细胞低于对照。所有白血病及正常人PBMC上HLA-ABC表达均为强阳性。在45例急性髓细胞白血病（AML）中，CD86阳性占18例（40％），CD86的表达在M4和M5亚型AML中最高；HLA-DR阳性25例（55％），HLA—DR在M2、M4、M5的表达明显高于其它亚型，而在M3型表达HLA-DR均为阴性；CD80、HLAABC在不同FAB亚型的表达无差异。CD86在高危核型及Ph＋组的表达低于低危核型组。共刺激分子及MHC分子的表达与诱导化疗的疗效未发现有相关。结论：各型白血病存在不同程度的B7或HLA-DR表达的缺陷。上调HLA-Ⅱ抗原及协同刺激分子在白血病细胞上的表达对设计高效的白血病免疫治疗方案具有重要意义。     

CD7+CD56+双阳性急性髓系白血病临床生物学特征

目的：探讨CD7^＋CD56^＋急性髓系白血病（AML）的临床生物学意义。方法：对25例初治CD7^＋CD56^＋AML患者进行细胞学形态、免疫表型、多药耐药P糖蛋白（PgP）检测，临床观察、并常规采用HAE方案诱导治疗，判定疗效，并随机选择66例CD7^-CD56^-AML患者进行对照。结果：CD7^＋CD56^＋AML阳性率4．08％（25／612）。CD7^＋CD56^＋AML在FAB分型中以M0、M1、M5、M7多见。与CD7^-CD56^-AML组比较CD7^＋CD56^＋AML具有高血红蛋白含量（89．29：75．62g／L，P〈0．05），高表达PgP（78．26％：34．85％，P〈0．01）和CD34表达（72．00％：45．45％，P〈0．05）等特征；此外，CD7^＋CD56^＋AML患者中枢神经系统浸润现象明显（36．00％：3．27％，P〈0．01），CD7CD56共表达与年龄、性别、白细胞计数、血小板计数、及外周血幼稚细胞数无关，也不影响完全缓解率和无病生存时间（均P〉0．05）。结论：CD7^＋CD56^＋AML具有独特的临床生物学特征，较少贫血，高表达PgP和CD34，常伴有中枢神经系统浸润。     

210例具有11q23染色体异常的急性髓系白血病的临床分析

目的:研究伴11q23染色体异常的成人急性髓系白血病(AML)的形态学、免疫学和临床特征。方法:对210例初治AML患者进行回顾性分析,包括细胞形态学、免疫表型、核型分析和临床资料。结果:13例AML患者存在11q23易位和缺失(发生率为6.19%),其中6例为M5a,4例为M5b,M4Eo、M3和M2各占1例。免疫表型检测显示伴11q23异常的患者除了高表达造血干/祖细胞标志分子CD34和CD117等外,通常高表达单核系统相关抗原,如CD14、CD15和CD11b。伴11q23异常组的化疗完全缓解率与正常核型对照组无明显差异(P>0.05),但无病生存期低于正常核型对照组(P<0.01)。结论:伴11q23异常的AML占所有AML的6.19%,似与单核细胞的分化阻滞相关,临床预后不良。     

急性髓系白血病M4/M5亚型的临床和遗传学研究

目的研究伴11q23异常的急性粒单细胞和单核细胞白血病患者的临床和细胞遗传学特征。方法用染色体G显带和间期荧光原位杂交技术对30例急性髓系白血病（AML）-M4、M5患者进行染色体检测,患者均接受柔红霉素、阿糖胞苷为主的化疗方案,并对其随访。结果伴11q23异常13例,其中M59例（M5a1例、b15b8例）、M4b5例;异常核型为t（11;19）、t（11;17）、t（9;11）、t（10;11）、t（6;11）、t（11：？）（q23：）、del（11）（q23）。混合细胞白血病（MLL）基因阳性13例,其中hi58例、hi45例,其完全缓解（CR）率15．4％,低于MLL阴性者的57．0％;MLL阳性者中位生存期85d,低于MLL阴性者的130d。结论11q23异常以MLL．hi5、hi4患者发生率高,MLL阳性者CR率低,平均生存期短。提示MLL基因异常是MLL患者预后不佳的标志。     

老年CD+56急性髓系白血病临床生物学特征

目的 研究CD+56老年急性髓系白血病(AML)的临床生物学意义.方法 对102例初治老年AML进行细胞形态学、免疫表型、多药耐药P糖蛋白(PgP)检测,并常规采用HAE方案诱导治疗,判定疗效.结果 老年急性髓系白血病,CD56阳性率39.22%.CD+56AML在FAB分型中以M2b、M5、M7多见,高白细胞计数(57.03×109/L vs 33.65×109/L,P=0.047),多表达PgP(62.50% vs 40.32%,P=0.042).CD+56AML患者髓外浸润现象明显(62.50% vs 37.09%,P=0.015),尤其是脾脏(42.50% vs 19.35%,P=0.014)显著受累,CD56表达与年龄、性别、血红蛋白含量、血小板计数及外周血幼稚细胞数无关,也不影响CR率(P值分别为0.306,0.840,0.564,0.302,0.686,0.547),但无病生存时间(DFS)(5.75个月 vs 30.00个月,P=0.048)和总生存时间(OS)(5.34个月 vs 22.03个月,P=0.032)较短.结论 CD+56AML具有独特的临床生物学特征,多表达耐药蛋白PgP,生物学侵袭性较强,生存期短,预后较差.建议初诊时监测CD56分子表达以判断预后.     

164例非M3型急性髓系白血病免疫表型的临床预后研究

目的 :探讨非M3型急性髓系白血病(AML)患者免疫表型的一般临床特征及预后相关性。方法 :采用CD45/侧向角散射(SSC)设门十色荧光标记流式细胞术,检测164例AML(非M3)患者抗原CD2、CD4、CD7、CD19、CD79a、CD11b、CD13、CD15、CD33、CD64、CD14、CD117、髓过氧化物酶(MPO)、人类白细胞DR抗原(HLA-DR)、CD34、CD38、CD56的表达。回顾分析不同免疫表型与年龄,性别,法国、美国和英国(FAB)分型,初诊时白细胞(WBC)、血小板(PLT)、血红蛋白(Hb)及预后的关系。结果:在164例AML(非M3)患者中髓系相关抗原表达率依次是CD13(97.6%)、CD33(97.6%)、CD117(89.6%)和MPO(84.8%);与祖相关抗原表达率依次是CD38(92.7%)、HLADR(84.8%)、CD34(63.4%),部分AML患者伴有淋系相关抗原表达,表达率最高的是CD7(30.5%),其次分别是CD56(22.0%)、CD4(18.3%)、CD19(9.8%)。CD19+、CD56+的AML患者中,M2多见,其中CD19+尤多见于M2b患者中,且CD19+、CD56+患者完全缓解(CR)率显著高于CD19-、CD56-的患者(P=0.048、P=0.038)。56.7%的AML患者具有白血病相关抗原表型(LAIP)阳性,以M2、M4、M5为主,LAIP表现为抗原跨系列表达(约87.1%,以CD7+CD117+CD34+/-、CD56+CD117+CD34+/-为主)、抗原表达量异常(约32.3%,以CD33dim为主)、抗原非同步表达(约6.5%,以CD11b同期表达为主),其中,存在抗原非同步表达的AML患者显示较短的总生存(OS)期、无病生存(DFS)期,提示其预后较差。结论:免疫表型对预测AML患者预后及指导治疗有一定的价值。     

急性髓细胞白血病免疫表型分析

目的：分析成人初治急性髓细胞白血病（AML）髓系抗原、CD34及Pgp表达特点及其与预后的关系。方法：采用流式细胞仪免疫荧光标记法检测65例初治成人AML的免疫表型。结果（1）髓系抗原阳性率依次为CD33＞CD15＞CD13＞CD14,CD33阳性率高达98．46％。CD14在M5、M6表达率较高;（2）CD34及HLA－DR阳性表达率以M1、M5较高,M3最低;（3）P－糖蛋白（PG)阳性率58．33％,Pgp阳性AML的CR率28．57％,明显低于Pgp阴性的CR率（63．63％,P＜0．005）。结论AML的免疫表型检测髓系单抗可选择CD33、CD15和（或）CD14。CD34和HLA－DR低表达为M3的特征。Pgp表达与CR率有密切的关系。     

36例献血者献血后网织红细胞检测的结果分析

目的探讨急性髓细胞白血病(AML)细胞尿激酶型纤溶酶原激活物受体CD87(uPAR)的表达及其在诊断急性白血病分型、指导预测预后方面的意义。方法应用流式细胞术(FCM)检测了41例初治的AML患者(包括M12例,M217例,M45例,M517例),应用t检验及χ2检验分析CD87阳性与CD87阴性患者在临床表现、染色体异常及完全缓解率间的差异,应用logistic回归分析影响患者完全缓解的具有统计学意义的因素。结果41例AML患者,26例CD87阳性表达,CD87阳性与CD87阴性AML患者比较肝肿大比例分别为73%与40%,(P<0.05),而淋巴结肿大、脾肿大比例无明显的统计学意义(P>0.05);出血倾向比例分别为77%与46%,(P<0.05);染色体异常的比例分别为73%与40%,(P<0.05);1疗程完全缓解率分别为40%与73%,(P<0.05),CD87阳性是导致患者完全缓解率低的独立因素。结论CD87表达有助于AML的诊断,CD87阳性与疾病进展包括浸润、出血、缓解率低等不良预后相关。     

CD_(116)在急性白血病中的表达及临床意义

目的 :探讨 CD1 1 6 在急性白血病中的表达及临床意义。方法 :对 114例急性白血病患者进行免疫表型及细胞遗传学分析。结果 :CD1 1 6 在急性淋巴细胞白血病 (AL L )中无阳性表达 ,而在急性髓性细胞白血病 (AML )中阳性表达率为 42 .4% ;CD1 1 6 在 AML各亚型间出现的频率存在明显差异 ,阳性率 M5 为 83.3% ,M4为 40 .0 % ,M3和 M2 分别为 2 7.2 %和 15 .0 %。 2例 M5 患者出现染色体 8异常 ,伴 CD1 1 6 阳性表达。结论 :CD1 1 6 主要在髓性细胞白血病中表达 ,且与具有单核细胞特征的白血病相关 ;CD1 1 6 联合 CD4有利于 M5 亚型白血病的诊断。     

急性单核细胞白血病M5a和M5b核型与临床特征的比较

目的比较急性单核细胞白血病M5a和M5b核型差异,并了解其与临床特征之间的相互关系.方法采用骨髓直接法和24 h短期培养法制备染色体标本,用G显带技术,对58例成人初发急性单核细胞白血病进行核型分析,同时对其临床资料进行回顾性研究.结果58例患者中正常核型28例,异常核型30例,其中,正常核型在M5b中出现率高于M5a(P＜0.01),异常核型中11q23异常和+8染色体在M5a中均较M5b常见(P＜0.01);临床上异常核型的M5患者常有高白细胞计数,中枢神经系统浸润,完全缓解率低及存活期明显缩短的特征.结论急性单核细胞白血病在遗传和临床上是一组异质性疾病,但M5a和M5b仍具有各自独特的遗传学背景.     

Aberrant co-expression of CD19 and CD56 as surrogate markers of acute myeloid leukemias with t(8;21) in Taiwan

Aberrant antigen expression in acute myeloid leukemia (AML) has been extensively studied in the West with limited reports from Taiwan. We carried out this retrospective study to characterize the frequency and significance of aberrant antigen expression of AML in Taiwan. Among 111 cases, 58 (52%) showed aberrant antigen expression, most frequently CD7 (27%) and CD56 (23%). Aberrant CD7 expression was observed in all non-AML-M3 subtypes, most frequently in AML-M7 (4/6, 67%); while CD19 expression was only observed in AML-M2 (5/36, 14%). CD56 expression was most common in AML-M5 (4/8, 50%). The relative frequency of CD19 and CD56 expression in AML with t(8;21) was higher than those with other chromosomal abnormalities or normal karyotype (P = 0.011 and 0.005, respectively). In non-M3 AML, aberrant antigen expression was identified in 56/96 (58%) cases, in contrast to 2/15 (13%) AML-M3 cases (P = 0.001). CD7, CD19 and CD56 expression was not correlated with remission rate. We concluded that aberrant immunophenotype was more frequent in non-M3 leukemias in Taiwan. The relative frequency of CD19 and/or CD56 expression in AML with t(8;21) was significantly higher than those without this translocation and co-expression of these two antigens may serve as the surrogate markers for AML with t(8;21).     

系统检测慢性乙型肝炎患者外周血淋巴细胞免疫表型的临床意义

目的:系统研究慢性乙型肝炎患者外周血淋巴细胞免疫表型以及与临床的关系.方法:用流式细胞术测定28例慢性乙型肝炎患者外周血单个核细胞膜CD3,CD4,CD5,CD25,CD28及CD38等相关CD分子的表达情况,并与22例健康对照组比较,并分析其与HBVDNA及临床的相关性.结果:28例慢性乙型肝炎患者外周血中CD4 CD25 ,CD8 HLADR CD38 ,CD3-CD19 ,CD5-CD19 及CD19 CD38 淋巴细胞数明显高于健康对照组(t=2.37,3.71,4.10,2.31,2.17,P<0.05),而CD3-CD8 ,CD8 CD28-及CD3-CD(16 56) 淋巴细胞数明显低于健康对照组(t=3.14,3.20,2.51,P<0.05).外周血中HBVDNA含量>109copies/L的患者其CD3 CD8 ,CD8 CD28 ,CD4 CD45RA CD62L ,CD8 CD45RA CD62L 及CD4 CD38 淋巴细胞数均显著高于HBVDNA含量<109copies/L的患者,差别有统计学意义(t=2.16,2.42,2.83,3.01,2.50,P<0.01或P<0.05).结论:慢性乙型肝炎患者T、B两种淋巴细胞的活化程度均较高,NK细胞数量减少;体内HBV复制活跃的患者其T淋巴细胞活化程度较高.     

IgM myeloma: a rare entity characterized by a CD20-CD56-CD117- immunophenotype and the t(11;14)

IgM myeloma is a very rare and poorly defined entity. In a detailed assessment of 10 cases, it was demonstrated that 70% had an aberrant phenotype based on the expression of CD19, CD45, CD27 and Cyclin D1 but all cases lacked CD56 and CD117. Interphase fluorescence in situ hybridization demonstrated deletion 13 in 50% while 5/8 cases assessed had a t(11;14). Despite the high incidence of the t(11;14), CD20 was only expressed in one of nine cases. We conclude that IgM myeloma is a distinctive subset characterized by a CD20-CD56-CD117- phenotype and the t(11;14).     

MICM分型诊断在鉴别M2和M3型急性髓性白血病中的意义

目的：探讨形态学、免疫学、细胞遗传学和分子生物学(MICM)分型诊断在鉴别M2、M3型急性髓性白血病(AML)中的意义。方法：对10例按FAB方案难以区分M2、M3型的AML及2例在基层医院诊断为M3b，用全反式维甲酸(ATRA)治疗未获缓解的患者应用常规细胞遗传学(CC)进行核型分析；以筑巢式逆转录聚合酶链反应(nested—RT—PCR)技术检测PML／RARa及AML1／ETO融合基因转录本；以流式细胞术检测白血病细胞免疫表型。对2例在基层医院诊断为M3b而用ATRA治疗效果不好的病例用间期双色FISH技术检测AML1／ETO融和基因。结果：12例患者中，4例有t(8；21)．AML1／ETO融合基因转录本阳性，确诊为M2；2例有t(15；17)，PML／RARa融合基因转录本阳性，确诊为M3；其他6例患者为正常核型，其中，3例AML1／ETO阳性，确诊为M2；1例PML／RARa阳性，确诊为M3；2例PML／RARa及AML1／ETO均为阴性．1例免疫表型为CD13、CD33^ 、CD34^ 、CD19^ ，最后诊断为M2，另1例免疫表型为CD13^ 、CD33^ 、CD34^ 、CD19^ ．最后诊断为M3。2例行FISH检测的患者AML1／ETO融和基因均为阳性。结论：对形态学无法鉴别M2、M3的AML进一步进行细胞遗传学、分子生物学及免疫学检测，可提高确诊率，并为治疗提供可靠的依据。     

干扰素α-2b联合利巴韦林治疗慢性丙型肝炎患者肝内免疫细胞的变化

目的观察干扰素α-2b和利巴韦林联合治疗前后漫性丙型肝炎患者肝内免疫细胞动态变化情况，为研究免疫调节疗法提供依据。方法利用流式细胞计数仪对42例慢性丙型肝炎患者应用联合治疗前及其中11例治疗后患者末梢血和（或）肝脏组织进行分析。结果与对照组相比慢性丙型肝炎组肝脏内CD56^＋、CD57^＋、CD161^＋细胞及CD56^＋T淋巴细胞阳性率明显减少（P〈0．01），CD161^＋T淋巴细胞有减少倾向；CD56^＋T淋巴细胞表达的CD28可见减少，CD152的表达可见增加（P〈0．05）；CD83^＋CD1a^＋细胞阳性率有减少倾向，CD80^＋CD11c^＋、CD86^＋CD11c^＋细胞阳性率明显减少（P〈0．01）；显效组减低的CD56^＋、CD161^＋、CD56T、CD161^＋T、CD80^＋CD11c^＋、CD86^＋CD11c^＋细胞治疗后可见增加。结论慢性丙型肝炎患者肝脏内自然杀伤细胞、自然杀伤T淋巴细胞数量及树突状细胞数量和功能减低，联合治疗使细胞免疫功能的抑制得到了改善。     

Mixed phenotype acute leukemia of T/myeloid type with a prominent cellular heterogeneity and unique karyotypic aberration 45,XY, dic(11;17)

Introduction. A 26‐yr‐old male patient with mixed phenotype acute leukemia of T/myeloid type with prominent leukemic cell heterogeneity, and the presence of a so far unreported karyotype aberration in this type of acute leukemia 45,XY, dic(11;17)(11qter→11p11.2::17p11.2→17qter) is presented. Methods. Flow immunocytometry was performed by direct multicolor immunofluorescent technique on bone marrow aspirates. Cytogenetic analyses were performed using G‐banding method by direct preparation of unstimulated bone marrow cells and following 24 hours of culture in RPMI 1540 culture medium with 25% fetal calf serum at 37°C Results. The flow immunocytometry of bone marrow nucleated cells revealed the existance of three distinct blast cell populations with overlapping immunophenotypes. Predominant blast cell population had an early myeloid phenotype and aberrant expression of CD7 antigen (HLA‐DR⁺, CD34⁺, anti‐MPO⁺, CD117⁺, CD33⁺, CD13⁺, CD7^+low, cyCD3^?, TdT^?). The other two blast cell populations, smaller in cell diameter and less sizable in cell proportion, both shared the T‐lymphoid features. The patient was treated with ADE protocol (etoposide, cytarabine and doxorubicine). A complete remission was achieved and lasted 5 months. Conclusion. A case of MPAL with complex biological features, 45,XY, dic(11;17)(11qter→11p11.2::17p11.2→17qter) karyotype and an aggressive, therapy‐resistant clinical course, is presented.     

Analysis of NPM1 Gene Mutations in Chinese Adults with Acute Myeloid Leukemia

Many European groups have recently described that mutations at exon-12 of the nucleophosmin (NPM1) gene are the most frequent genetic lesion in patients with acute myeloid leukemia (AML), especially in the presence of a normal karyotype. This study explored the prevalence and clinical profile of NPM1 mutations in a cohort of 156 Chinese adults with AML. NPM1 exon-12 mutations were detected using direct sequencing or fragment analysis of genomic DNA polymerase chain reaction products. NPM1 mutations were present in 28.2% of the overall population, including 1/1 (100%) of M0, 11/27 (40.7%) of M1, 11/46 (23.9%) of M2, 0/29 (0%) of M3, 2/9 (22.2%) of M4, 18/39 (46.2%) of M5, and 1/5 (20.0%) of M6. NPM1 gene mutations were more prevalent in patients with a normal karyotype (37 of 90; 41.1%) when compared with patients with karyotypic abnormalities (7 of 66; 10.6%;P < .001). Sequence analysis of 25 NPM1-mutated cases revealed known mutations (type A, D, N(M), and P(M)) as well as one novel sequence variation (here named as type S). All mutational types were heterozygous and showed a 4 bp insertion. NPM1 mutations were significantly associated with old age (P < .05), high peripheral white blood cell count (P < .05), and the subtypes of French-American-British categories M1/M5, but negatively associated with expression of CD34 (P < .05) and CD117 (P < .05). Thus, this study provides the methods of NPM1 exon-12 mutations detection and related clinical data of NPM1 mutated cases in a Chinese population.     

Adverse prognostic significance of CD20 positive Reed-Sternberg cells in classical Hodgkin's disease

The prognostic significance of CD20 positive classical Hodgkin's disease (cHD) is uncertain. All cHD cases referred to the Memorial Sloan-Kettering Cancer Center (MSKCC) were retrospectively identified (5/92-11/00); the samples were immunostained, and clinical data ascertained. Cases were re-reviewed without knowledge of clinical outcome. Univariate and multivariate analyses were performed 248 patients had cHD: 28 CD20(+) (11%); 220 CD20(-). All clinical characteristics were comparable except haemoglobin level at presentation. With a median follow-up of 29.2 months, significant prognostic factors in multivariate analysis were: CD20 positivity, elevated white blood cell count (WBC) and low absolute lymphocyte count for time-to treatment failure (TTF); and for overall survival (OS), CD20 positivity, elevated WBC count, bone marrow involvement and age >/=45 years. TTF was significantly poorer for ABVD-treated patients with CD20(+) cHD as compared with CD20(-) cHD. Among 167 patients treated at MSKCC, both TTF (P < 0.0001) and OS (P = 0.017) were significantly decreased in CD20(+) patients as compared with CD20(-) cHD. CD20(+) cHD is a poor prognostic factor for TTF and OS. All cHD cases should be immunophenotyped for CD20. A large prospective trial is needed to confirm these findings.     

Abnormality of bone marrow-derived mesenchymal stem cells in patients with systemic lupus erythematosus

Bone marrow-derived mesenchymal stem cells (MSCs) are key components of the hematopoietic microenvironment and provide support to hematopoiesis and modulate immune system. Several studies suggest that SLE may be seen as stem cell disorders. However, it is unclear that whether MSCs from SLE patients are defective. So in this research, we studied the biological character of bone marrow derived MSCs in patients with SLE, focused on their phenotype (morphology and immunophenotype), karyotype, cytokines expression and hematopoietic support of MSCs. Our results showed that MSCs from SLE patients and normal controls can be successfully culture-expanded, but the MSCs from SLE grew more slowly than those of normal controls (P < 0.05). Cells from both groups were positive for CD29, CD44 and CD105, and negative for CD14, CD34, CD45 and HLA-DR. MSCs from SLE have a normal karyotype. Both groups express IL-6, IL7, IL-11, macrophage colony stimulating factor (M-CSF) and stem cell factor (SCF) at mRNA level. While IL-6 and IL-7 were down-regulated in MSCs from SLE patient (P < 0.05) at mRNA level. The MSCs from SLE patients and normal controls were infused into ICR (Tac: Icr: Ha strain) mice after high-dose chemotherapy, with no adverse events in either group. Recovery of white blood cells, hemoglobin and platelet was more rapid (P < 0.05) compared with the group without MSCs infusion. We conclude that MSCs in patient with SLE have abnormalities compared with those in normal control. MSCs in patient with SLE may play an important role in the SLE pathogenesis.