CpG寡核苷酸诱导人外周血单核细胞抗膀胱肿瘤BIU-87细胞的杀伤作用

目的 研究A型与B型CpG ODN对人外周血单个核细胞(PBMC)的增殖,细胞因子的释放和诱导人PBMC抗膀胱肿瘤细胞作用.方法 用A型、B型CpG ODN和NoCPG ODN刺激正常人外周血PBMC,MTT测定细胞的增殖,定量ELISA检测人干扰素-α含量,LDH法检测CpG ODN诱导后人PBMC对膀胱肿瘤细胞的杀伤作用.结果 A型与B型CpG ODN对人PBMC增殖的刺激作用明显高于对照组;CpGODN2216组IFN-α的浓度高于CPG ODN2006组;CpG寡核苷酸作用后,人PBMC对BIU-87膀胱肿瘤细胞的杀伤活性明显升高.结论 A型与B型CpG ODN对人PBMC具有免疫诱导作用,可刺激人PBMC增殖并释放IFN-α,诱导免疫细胞对膀胱肿瘤细胞杀伤,增强宿主抗膀胱肿瘤细胞作用.     

人枯否细胞在同种肝移植免疫中作用机制初步探讨

目的 探讨肝脏枯否细胞(KC)在肝移植后早期免疫反应中的可能作用.方法 将KC和(或)异体PBMC共培养,收集细胞上清液,培养结束时分别收获培养的KC和PBMC.检测HLA-G在细胞表面的表达;测定上清液中NO、IFN-γ、IL-10和TGF-β1的浓度;MTT试验观察KC对淋巴细胞增殖的影响.结果 实验组及对照组中KC和PBMC表面均未检测到HLA-G的表达.与不含KC实验组相比,含KC实验组中,NO、IL-10和TGF-β1的产量显著升高,而IFN-γ呈相对偏低趋势;对照组中未能检测到IL-10和IFN-γ的分泌,仅含KC的对照组中含少量NO及TGF-β1,且显著低于实验组.MTT实验发现,不含KC实验组OD值显著高于含KC实验组及对照组.结论 体外KC接触异体PBMC后早期,各细胞膜表面均无HLA-G表达,但参与了NO及Th2/Th3样细胞因子的分泌调节,并能抑制淋巴细胞增殖反应,可能促进肝脏移植早期免疫耐受的形成.     

氩氦刀冷冻联合CpG寡脱氧核苷酸治疗小鼠皮下移植性结肠癌

目的 探讨氩氦刀冷冻消融联合CpG寡脱氧核苷酸（ODN）对小鼠移植性结肠癌的治疗作用.方法 BALB/c小鼠皮下接种结肠癌CT26细胞建立荷瘤鼠模型,小鼠被分成PBS组（6只,瘤周注射PBS组）、氩氦刀组（6只,氩氦刀冷冻组）、CpG ODN组（6只,瘤周注射CpG ODN）和联合治疗组（6只,氩氦刀冷冻加瘤周注射CpG ODN）.观察各组小鼠存活及肿瘤生长情况;采用酶联免疫吸附试验检测小鼠外周血中IL-12和IFN-γ的含量;利用流式细胞仪检测小鼠外周血中CD3＋CD4＋T细胞与CD3＋CD8＋T细胞比例;对氩氦刀组和氩氦刀联合CpG ODN组治愈小鼠进行再攻击实验,观察小鼠再次成瘤率.结果 氩氦刀组和联合治疗组小鼠的平均生存时间为（80.3±5.4）d和（83.8±5.5）d,明显长于PBS组[（53.7±3.7）d]和CpG ODN组[（51.5±6.8）d],差异均有统计学意义（P＜0.05）.氩氦刀组和联合治疗组抑瘤率分别为83.8%和86.2%.治疗后20 d,氩氦刀组和联合治疗组的CD3＋CD4＋T细胞/CD3＋CD8＋T细胞比值、IL-12和IFN-γ水平均高于PBS组和CpGODN组,差异有统计学意义（P＜0.05）;与氩氦刀组比较,联合治疗组CD3＋CD4＋T细胞/CD3＋CD8＋T细胞比值差异无统计学意义,但IL-12和IFN-γ水平则显著升高（P＜0.05）.肿瘤再攻击后,氩氦刀组和联合治疗组分别有5只（5/6）和1只（1/6）再次成瘤,差异有统计学意义（P＜0.05）.结论 氩氦刀冷冻联合CpG ODN可以增强荷瘤鼠的抗肿瘤免疫应答,增强了氩氦刀治疗小鼠的免疫功能,减少了肿瘤再次攻击的成瘤率.     

慢性HBV感染者外周血单个核细胞分泌干扰素α功能初探

目的：旨在检测慢性HBV感染者外周血单个核细胞（PBMC）分泌干扰素α（IFN-α）的情况,以探究其外周血浆细胞样树突状细胞（pDC）和单核细胞功能是否存在缺陷。方法前瞻性纳入2012年7月至2013年3月北京协和医院肝炎门诊就诊的慢性乙型肝炎（CHB）患者16例,同期选取与之年龄相匹配的HBV携带者16例和健康人18例。采集血样,分离PBMC,分别与含未甲基化的胞嘧啶鸟嘌呤二核苷酸序列的寡脱氧核苷酸2216（CPG ODN2216）、聚肌苷酸胞苷酸（poly I：C）刺激共培养,并用酶联免疫吸附试验（ELISA）测量其分泌IFN-α量。结果经ODN2216刺激后,CHB组患者PBMC分泌IFN-α量平均为31.20（7.33～44.04）pg/ml,HBV携带者组PBMC分泌IFN-α量平均为109.91（13.74～240.27）pg/ml,健康对照组PBMC分泌IFN-α量平均为107.95（48.59～227.33）。CHB患者组显著低于健康对照组,差异具有统计学意义（Z=-2.691,P=0.007）。CHB患者组显著低于HBV携带者组,差异具有统计学意义（Z=-2.206,P=0.027）。经poly（I：C）刺激后,三组PBMC分泌IFN-α量差异无统计学意义（F=0.628,P=0.427）。结论较HBV携带者和健康对照组,CHB患者体内PBMC中树突状细胞分泌IFN-α明显下降,而单核细胞分泌IFN-α量无显著性降低。     

α1,3-半乳糖基转移酶基因沉默对NK细胞介导的异种细胞毒作用的影响

目的 探讨α1,3-半乳糖基转移酶(α1,3-GT)基因沉默对人自然杀伤(NK)细胞介导的异种细胞毒作用的影响.方法 将培养的永生化猪血管内皮细胞系细胞株PED分为3组.转染组:PED转染了特异性α1,3-GT 核糖核酸干扰分子(SiRNA-1);错配组:PED转染了错配的SiRNA;空转染组:PED未转染SiRNA.观察各组PED与人NK细胞系细胞株NK 92在静止和流动状态下的粘附作用、不同效靶比下的NK92细胞毒作用以及PED和NK 92混和培养上清液中γ干扰素(IFN-γ)的水平.结果 PED转染后48 h,转染组、错配组和空转染组在静止状态下粘附NK92的数量(个)分别为262±26、275±24和252±23;流动状态下分别为132±12、125±15和110±20,无论是静止还是流动状态下,各组PED对NK92的粘附能力的比较,差异均无统计学意义(P＞0.05).无论PED是否被活化,在相同效靶比下NK92对各组PED的杀伤率的比较,差异均无统计学意义(P＞0.05),但杀伤率与效靶比呈正相关.NK92与PED共孵育早期即有反应性IFN-γ分泌,其分泌水平[(366.9±28.7)ng/L]较其自发分泌水平[(60.1±6.4)ng/L]增加了5倍,在共孵育后12 h分泌值最高,但各组间不同时段IFN-γ分泌值的比较,差异均无统计学意义(P＞0.05).结论 利用RNA干扰技术下调PED上的α1,3-半乳糖残基(α-Gal)的表达,未引起NK92和PED相互作用的明显改变.α-Gal可能并非是NK细胞作用的靶位点,其表达量的高低对NK细胞的活化、粘附及杀伤能力未产生负性影响.     

小鼠肠移植术前输注表达吲哚胺2,3双加氧酶的供者树突细胞抑制排斥反应

目的观察干扰素γ(IFN-γ)诱导供者(C57BL/6小鼠)脾树突细胞(DC)表达吲哚胺2,3双加氧酶(IDO)的情况;研究受者(BalB/c小鼠)小肠移植术前输注高表达IDO的供者DC对排斥反应的抑制作用。方法用IFN-γ诱导供者DC表达IDO;半定量逆转录聚合酶链反应、免疫印迹法及毛细管电泳法检测IDO表达水平及活性,混合淋巴细胞培养(MLR)测定IDO刺激T细胞增殖的能力。利用小鼠异位小肠移植模型,设单纯移植组、DC输注移植组(术前输注供者脾DC 2×10~6个)及诱导DC输注移植组(术前输注经IFN-γ诱导的供者脾DC 2×10~6个),术后观察移植肠存活时间并行病理学检查。结果经IFN-γ诱导的脾DC IDO分子mRNA转录水平(相对量)、IDO蛋白表达水平(相对量)及培养液中犬尿氨酸浓度分别为(1.23±0.02)、(2.74±0.01)以及(76.52±0.44)μmol/L,未经IFN-γ诱导的脾DC分别为(1.05±0.05)、(1.40±0.17)及(43.31±0.48)μmol/L,前者显著增强(P<0.01)。脾DC对同种T细胞增殖的刺激作用在IFN-γ诱导后减弱,在加入IDO的特异性抑制剂后增强。输注诱导DC移植组移植肠中位存活时间(12 d)较单纯移植组(6 d)及输注DC移植组(7.5 d)显著延长(P<0.01),而移植肠病理分级显著性降低(P<0.05)。结论IFN-γ可诱导小鼠脾DC高表达活性的IDO,后者可减弱DC刺激T细胞增殖的能力。受者术前输注高表达IDO的供者DC能够诱导针对供者的特异性免疫耐受而减轻排斥反应。     

肝囊型包虫病患者外周血单个核细胞表面程序性死亡受体配体1的表达及其与干扰素-γ的关系

目的 探讨肝囊型包虫病患者外周血单个核细胞(PBMC)表面程序性死亡受体配体1(PD-L1)的表达及其与血清1FN-γ水平之间的关系.方法 回顾性分析2010年6月至2011年2月新疆医科大学第一附属医院收治的63例肝囊型包虫病患者的临床资料.根据世界卫生组织包虫病专家组包虫病标准化分型原则将患者分为肝包虫活性组(38例)和肝包虫无活性组(25例),20例肝血管瘤患者及健康志愿者作为正常对照组.采用流式细胞仪及免疫组织化学法检测PD-L1阳性表达率,ELISA法检测血清IFN-γ的表达水平.组间比较采用成组设计资料￡检验和单因素方差分析,进一步两两比较采用LSD检验,总体分布采用x2检验,PD-LI阳性表达率和IFN-γ的表达水平的相关性分析采用Pearson检验.结果 流式细胞仪检测肝包虫活性组、肝包虫无活性组和正常对照组PBMC表面PD-L1的阳性表达率分别为12.1％士3.8％、10.9％士2.5％和9.1％±2.5％,肝包虫活性组与正常对照组PD-L1的阳性表达率比较,差异有统计学意义(t =3.327,P＜0.05).免疫组织化学检测肝包虫活性组、肝包虫无活性组和正常对照组PBMC涂片中PD-L1的阳性表达率分别为11.9％±3.4％、10.6％±2.9％和9.5％±3.6％,肝包虫活性组与正常对照组PD-L1的阳性表达率比较,差异有统计学意义(t=2.470,P＜0.05).肝包虫活性组、肝包虫无活性组和正常对照组血清IFN-γ表达分别为(141±38) μg/L、(124±32) μg/L和(105±42) μg/L,肝包虫活性组与正常对照组IFN-γ表达水平比较,差异有统计学意义(t=3.280,P＜0.05).流式细胞仪和免疫组织化学检测PBMC的PD-L1阳性表达率与血清IFN-γ表达水平均呈明显正相关(r=0.59,0.61,P＜0.05).结论 PD-L1可能在IFN-γ的作用下发挥着促进肝包虫免疫逃避的重要作用.     

核因子-κB对小鼠树突状细胞分化成熟及其体外刺激T细胞免疫反应的影响

目的 探讨在小鼠树突状细胞(DC)成熟过程中核因子-κB(NF-κB)基因的作用。方法应用特异性NF-κB寡聚脱氧核苷酸诱骗剂(NF-κB ODN Decoys)阻断NF-κB活性，观察DC形态、细胞表面分子表达以及同种T淋巴细胞增殖反应的变化，了解NF-κB基因对DC成熟及免疫生物活性的影响。结果 NF-κB ODN Decoys的有效摄取，抑制了DC表面共刺激分子CD80、CD86、CD40的表达和白细胞介素-12(IL-12)的分泌，阻碍了DC的发育成熟，这种阻碍作用不可被脂多糖(LPS)所逆转。混合淋巴细胞反应显示，NF-κB ODN Decoys的应用可诱导DC刺激同种T淋巴细胞低反应活性，抑制了T细胞IL-2和γ-干扰素(IFN-γ)的分泌。结论 NF-κB是DC发育成熟过程中关键性调控基因。应用NF-κB ODN Decoys可抑制DC的成熟，从而为生成耐受原性未成熟DC、诱导移植免疫耐受提供了一种新的途径。     

白细胞介素-12基因修饰对树突状细胞表面分子表达及细胞因子分泌的影响

目的 观察白细胞介素(IL)-12基因修饰对树突状细胞(DC)表面分子及细胞因子分泌的影响.方法 采用重组逆转录病毒介导IL-12基因修饰人外周血单个核细胞(PBMC)来源的Dc;ELISA法检测各组DCs和各组T细胞上清中IL-12、IL-10、IFN-γ因子的分泌水平;流式细胞仪(FACS)分析各组DC表面CD83、CD86的表达;MTT法检测DC刺激同源T淋巴细胞增殖的能力;统计学分析比较各组间的差异.结果 IL-12基因修饰使得DC高表达CD83和CD86分子,分泌高水平IL-12及IFN-γ,但对IL-10因子的分泌无明显影响,刺激同源T淋巴细胞增殖明显,诱导激活的T细胞上清中IFN-γ水平显著增高、IL-10分泌水平显著降低.结论 经IL-12基因修饰后的DC表型成熟,分泌IL-12及IFN-γ的能力增强,对IL-10因子的分泌无影响,能抑制T细胞分泌IL-10因子,优化抗原提呈的微环境.     

骨髓移植小鼠急性移植物抗宿主病早期弥漫性肺损伤中TH17细胞的作用

目的 探讨骨髓移植小鼠急性移植物抗宿主病(aGVHD)早期肺损伤中TH 17细胞的作用和机理.方法 Balb/c小鼠为受鼠,经致死量全身照射(TBI)后,输注C57BL/6小鼠来源的骨髓细胞和脾细胞,建立aGVHD模型.实验分为3组:TBI组小鼠仅接受TBI,异基因骨髓移植(BMT)组小鼠TBI后输注供者骨髓细胞和脾细胞,常山酮(HF)组小鼠TBI后输注骨髓细胞和脾细胞,并注射HF.动态观察小鼠GVHD的表现,并进行肺组织病理学、T淋巴细胞亚群及相关细胞因子的检测.结果 移植后小鼠出现典型GVHD的表现.移植后6d时HF组肺组织病理学评分为(2.00±0.35)分,BMT组为(0.67±0.07)分.BMT组TH 1细胞占CD4+T淋巴细胞的比例为(5.53±0.11)％,TH 17细胞占(1.04±0.34)％;HF组TH1细胞占(8.61±0.21)％,TH 17细胞占(0.49±0.07)％;组间比较,差异有统计学意义(P＜0.05).两组均未检测到TH2细胞.移植后6d,BMT组白细胞介素(IL)-17A为(2.81±0.19)pg/ml,γ干扰素(IFN-γ)为(42.97±0.23) pg/ml; HF组IL-17A＜0.8 pg/ml,IFN-γ为(9.89±0.51)pg/ml;组间比较,差异有统计学意义(P＜0.05).两组均未检测到IL-10.结论 在异基因造血干细胞移植早期阻断TH17细胞及其细胞因子的分泌,导致炎症因子分泌失衡,加重肺损伤.     

Microtopography of metal surfaces influence fibroblast growth by modifying cell shape, cytoskeleton, and adhesion.

Stainless Steel (SS), titanium (cpTi), and Ti-6Al-7Nb (TAN) are frequently used metals in fracture fixation, which contact not only bone, but also soft tissue. In previous soft tissue cytocompatibility studies, TAN was demonstrated to inhibit cell growth in its "standard" micro-roughened state. To elucidate a possible mechanism for this inhibition, cell area, shape, adhesion, and cytoskeletal integrity was studied. Only minor changes in spreading were observed for cells on electropolished SS, cpTi, and TAN. Cells on "standard" cpTi were similarly spread in comparison with electropolished cpTi and TAN, although the topography influenced the cell periphery and also resulted in lower numbers and shorter length of focal adhesions. On "standard" microrough TAN, cell spreading was significantly lower than all other surfaces, and cell morphology differed by being more elongated. In addition, focal adhesion numbers and mean length were significantly lower on standard TAN than on all other surfaces, with 80% of the measured adhesions below a 2-microm threshold. Focal adhesion site location and maturation and microtubule integrity were compromised by the presence of protruding beta-phase microspikes found solely on the surface of standard TAN. This led us to propose that the impairment of focal adhesion numbers, maturation (length), and cell spreading to a possibly sufficient threshold observed on standard TAN blocks cell cycle progress and eventually cell growth on the surface. We believe, as demonstrated with standard cpTi and TAN, that a difference in surface morphology is influential for controlling cell behavior on implant surfaces.     

Rituximab, Anti-CD20, Induces In Vivo Cytokine Release But Does Not Impair Ex Vivo T-Cell Responses

Pre-formed HLA antibodies (Ab), reported as panel-reactive antibody (PRA), prolong transplant waiting time. We hypothesized that rituximab (RIT) could reduce PRA via B-cell depletion. As part of a Phase I study of single RIT dose, we studied in vivo and ex vivo effects on T-cell immune responses. Nine subjects (n = 3) were treated at 50, 150, and 375 mg/m(2). Serum interleukin-1alpha (IL-1alpha), IL-6, IL-12, tumor necrosis factor beta (TNF-beta), and interferon-gamma (IFN-gamma) were measured by enzyme-linked immunosorbent assay (ELISA). T-cell function was monitored with T-cell proliferation assays. IL-6 levels rose in eight patients (7.15 +/- 4.38 pg/mL to 86.22 +/- 77.08, p = 0.021). The high-dose group had detectable TNF-betapost rituximab infusion (874.7 +/- 1466.5 pg/mL). There was no decline in T-cell proliferation in response to phytohemagglutinin or allogeneic lymphocyte stimuli. Stimulation indices in the presence of both concentrations of tetanus toxoid rose significantly at 4 weeks.     

Renal tumors: The good, the bad, and the ugly

Renal cancers comprise a wide variety of neoplasms with quite different genetic and molecular characteristics and clinical behaviors. Several issues of significant note have arisen in association with our increased understanding of these tumors, including questions regarding early diagnosis, the evaluation of cystic lesions, the behavior of tumors occurring in young patients, and insights regarding the prognosis and best follow-up strategies for these tumors.     

Effect of norcantharidin on the proliferation,apoptosis, and cell cycle of human mesangial cells

Aims: Norcantharidin (NCTD) regulates immune system function and reduces proteinuria. We sought to investigate the effect of NCTD on proliferation, apoptosis and cell cycle of cultured human mesangial cells (HMC) in vitro.

Methods: HMC cells were divided into a normal control group, and various concentrations of NCTD group (2.5, 5, 10, 20, or 40?μg/mL). Cell proliferation was determined by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, apoptosis was detected by Annexin V/propidium iodide (PI) assays, and morphological analysis was performed by Hoechest 33258 staining. Finally, cell cycle was analyzed by flow cytometry.

Results: NCTD dose and time dependently inhibits HMC proliferation significantly (p?Conclusion: NCTD inhibits HMC cell proliferation, induces apoptosis, and affects the cell cycle.     

Expression of PCNA, p53, Bax, and Bcl-X in oral poorly differentiated and basaloid squamous cell carcinoma: relationships with prognosis

BACKGROUND: The aim of this study was to compare the clinical features and proliferating cell nuclear antigen (PCNA), p53, Bcl-X, and Bax expression in primary oral basaloid squamous cell carcinoma (BSCC) and poorly differentiated squamous cell carcinoma (PDSCC) matched by stage and site and to assess the possible prognostic significance of these variables. METHODS: Seventeen cases of oral BSCC were compared with 27 PDSCCs matched by stage and tumor site. In addition, PCNA, p53, Bax, and Bcl-X expression in both carcinomas were evaluated in relation to their clinicopathologic features and prognostic values using the Kaplan-Meier method and Cox regression models. RESULTS: No statistically significant differences were found between the groups (BSCC and PDSCC) in regard to clinical features and immunohistochemical reactivity for antibodies PCNA, p53, and Bcl-X. In comparison with PDSCC, the BSCC group exhibited a higher Bax score (p = .031). The 5-year and 10-year overall survival, cancer-specific survival, and disease-free survival rates demonstrated no significant differences between the BSCC and PDSCC groups, and the PCNA, p53, Bax, and Bcl-X also showed no prognostic value. CONCLUSIONS: These results suggest that the clinical and biologic course of BSCC is similar to PDSCC in the oral cavity when clinical stage and site are matched.     

Cell proliferation, apoptosis, angiogenesis and growth rate of incidentally found renal cell carcinoma

BACKGROUND: Our previous study showed that the growth rate of incidentally found renal cell carcinoma (RCC) varied, and that the initial clinical and pathological features did not predict subsequent growth of the carcinoma. The objective of this study was to determine the relationships between cell proliferation, apoptosis, angiogenesis and the growth rates of these RCC. METHODS: We examined cell proliferation, apoptosis, and angiogenesis in 16 incidentally found cases of RCC. Cell proliferation was assessed by immunohistochemical staining with a Ki-67 antibody. Apoptosis was assessed by the terminal deoxynucleotidyl transferase (TdT) mediated deoxy-UTP biotin nick end labeling (TUNEL) technique. The Ki-67 labeling index (KI) and the apoptotic index (AI) were determined as the ratio of immunohistochemically positive cells per 1000 cancer cells. The KI/AI ratio was also determined. Angiogenesis was evaluated by CD34 immunostaining. Finally, we investigated the correlation between these parameters and the growth rate of primary lesions of incidentally found RCC. RESULTS: The KI ranged from 7 to 73 (median, 20), AI ranged from 6 to 171 (median, 26), and microvessel density (MVD) ranged from 21 to 673 (median, 265) for incidentally found RCC. Ki-67 labeling index, AI and MVD were not closely correlated to each other. Furthermore, these parameters were not associated with growth rates of incidentally found RCC. Only the KI/AI ratio was strongly correlated to the growth rate of incidentally found RCC (r = 0.709; P = 0.0083). CONCLUSION: Our results suggest that the balance between cell proliferation and apoptosis partly determines the growth rate of primary lesions of incidentally found RCC.     

大鼠肝窦内皮细胞分离、培养及其生物学特性的初步研究

目的　建立大鼠肝窦内皮细胞 (SEC)的原代分离、培养方法 ,并研究其生物学特性。方法　胶原酶灌注结合Percoll密度梯度离心加选择性贴壁的方法分离SEC ;用光镜、扫描电镜观察培养SEC的形态学变化及超微结构 ;用Ⅷ因子和CD14免疫细胞化学染色及RECA 1单抗间接免疫荧光法观察SEC表面分子的表达。结果　分离培养的SEC得率为 (2 .0 6± 0 .35 )× 10 7/只大鼠 ,活力≥ 92 % ,纯度达 90 % ;光镜下细胞形态典型 ,SEM下可观察到特征性的窗孔结构 ;Ⅷ因子染色阴性而CD14染色阳性 ,RECA 1单抗间接免疫荧光染色阳性。结论　分离培养的SEC细胞得率、活力及纯度较高 ,形态典型且具有一般细胞所没有的窗孔结构及表面标志 ,为其功能和作用机制的深入研究奠定了基础。     

Specific localization of the basigin protein in human testes from normal adults, normal juveniles, and patients with azoospermia

Basigin is a transmembrane protein belonging to the immunoglobulin superfamily. Specific localization of the protein in normal human testes, from those of a 2-year-old boy to those of a 50-year-old man, and in testes with Sertoli cell only syndrome and germ cell arrest, is reported. Basigin localization was determined using an immunohistochemical technique with an antibody against human basigin. In the normal adult testes, basigin was detected at the periphery of both spermatocytes older than zygotene and round spermatids. In the juvenile testes, it was expressed in accordance with the appearance of pachytene spermatocytes. In this study, pachytene spermatocytes were detected in an 11-year-old boy. Basigin was not expressed in immature testes with germ cells younger than pachytene spermatocytes, namely in testes from boys aged 2-9 years. In testes from adult patients with Sertoli cell only syndrome, basigin was expressed at the periphery of Sertoli cells, but localization was confined to the adluminal compartment of the seminiferous tubule. In testes with germ cell arrest, the protein was expressed on germ cells from pachytene spermatocytes to step 2 spermatids, where present. The results show that in the normal human testes basigin is expressed with the onset of spermatocyte differentiation. Because human basigin is expressed in adult testes with Sertoli cell only syndrome, the protein seems to be synthesized in Sertoli cells and expression continues after these cells dedifferentiate in the seminiferous epithelium.