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抗肿瘤单克隆抗体的高度特异性与杀伤细胞对肿瘤的细胞毒效应相互结合起来,是增强LAK细胞抗肿瘤作用的重要途径。本研究用化学连接法制备了既可识别淋巴细胞表面CD3抗原又可识别LiBr黑素瘤细胞表面肿瘤相关抗原的双特异性抗体CD3-HB8759。FACS分析证实,CD3-HB8759具有结合两种抗原的活性,4h^51Cr释放细胞毒实验结果表明,CD3-HB8759在诱导相可显著增强LAK对LiBr细胞的 相似文献
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抗肿瘤单克隆抗体的高度特异性与杀伤细胞对肿瘤的细胞毒效应相互结合起来,是增强LAK细胞抗肿瘤作用的重要途径。本研究用化学连接法制备了既可识别淋巴细胞表面CD3抗原又可识别LiBr黑素瘤细胞表面肿瘤相关抗原的双特异性抗体CD3-HB8759。FACS分析证实,CD3-HB8759具有结合两种抗原的活性。4h51Cr释放细胞毒实验结果表明,CD3-HB8759在诱导相可显著增强LAK对LiBr细胞的细胞毒效应,也能使非LAK细胞获得细胞毒性;在杀伤相加入CD3-HB8759对LAK细胞的细胞毒作用也具有促进作用。上述结果表明,CD3-HB8759是一种抗人黑素瘤的双特异性抗体,为体内应用提供了良好的实验基础。 相似文献
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T细胞耐受的诱导及其机理研究 总被引:3,自引:0,他引:3
目的 阐明抗原特异性 T 细胞无能的诱导条件、无能细胞的特性及其耐受的机理。方法 抗 B71 单抗与 Cs A 联用诱导抗原特异性 T 细胞无能, 通过3 H Td R 掺入法测定 T 细胞增殖和 M L R, 利用 R T P C R 检测细胞因子基因表达。结果 耐受 T 细胞与异体淋巴细胞比例为0 .01∶1时, 可显著抑制 M L R, 转染 B71 分子的 M D A453 和3 A O 能协同刺激 C D3 诱导的 T 细胞增殖,不表达 B7 分子的 M D A453 和3 A O 无此作用。 P H A、 C D3 单抗、 P M A+ A23187 可以逆转本试验所用诱导方法所致的 T 细胞的耐受状态。无能 T 细胞 I L2 和 I F Nγm R N A 不表达, 而 I L4 和 I L10 m R N A可表达。无能 T 细胞活化后, I L2 和 I F Nγm R N A 能够表达。结论 抗原特异性 T 细胞耐受是可以人为诱导的, 无能 T 细胞细胞因子基因格局向 T H2 细胞偏离。 相似文献
5.
点突变p53肽诱导肽特异性CTL的研究 总被引:1,自引:0,他引:1
目的探索点突变p53肽诱导细胞免疫应答的可能性,为其作为肽疫苗用于肿瘤免疫治疗提供实验依据。方法人工合成小鼠点突变p53肽P132F(LNKLFFQL,132Cys→Phe突变),与不完全弗氏佐剂(IFA)或RIBI佐剂(RAS)混合,皮下免疫C57BL/6小鼠,分离脾细胞体外用肽再刺激,诱导细胞毒T淋巴细胞(CTL),并以51Cr释放法检测其杀伤活性。结果P132F肽加上IFA或RAS免疫小鼠,均能诱导肽特异性CD8+CTL;低剂量重组白细胞介素2(rIL-2)能增强肽免疫效果。结论所用突变的p53蛋白具有免疫原性,提示来源于突变p53的抗原肽有可能作为肽疫苗用于临床肿瘤免疫治疗 相似文献
6.
CD4+T细胞在痢疾疫苗诱导小鼠肠粘膜免疫应答中的作用 总被引:1,自引:0,他引:1
以本室构建的双价痢疾候选疫苗株FS5416 作为口服免疫原,检测了小鼠PP 结(Peyer ,s patches) 中T 淋巴细胞的体外增殖反应, 观察了腹腔注射抗L3T4 m Ab 对小鼠肠粘膜部位产生特异性Ig 分泌细胞的影响。结果表明:①小鼠口服免疫后,PP 结中的CD4 + T 细胞可产生明显的特异性增殖反应:②选择性地删除CD4 + T 细胞后,小鼠肠粘膜无抗原特异性Ig 分泌细胞产生。以上提示,小鼠肠粘膜对痢疾疫苗的免疫应答需要CD4 + T 细胞的参与。 相似文献
7.
合成多肽体外诱导乙肝病毒抗原特异性CTL杀伤机制研究 总被引:3,自引:0,他引:3
为探讨合成多肽体外诱导乙肝病毒抗原特异性T细胞杀伤机制,应用免疫组化检测HGV-CTLsFas配体表达情况,燕分析培养上清一氧化氮含量与细胞毒活性的关系。结果显示,HBV-CTLs对转染HBV DNA的肝癌细胞存在明显的特异性细胞毒活性,其Fas配体表达阳性率分别为58%,56%,明显高于CD3-AK细胞组,细胞培养上清NO含量动态分析显示,HBV-CTLs细胞培养上清NO含量与细胞毒活性存在正相 相似文献
8.
本实验检查了门脉注射异基因脾细胞后,受体鼠耐受的诱导及其可能的机制。结果表明,门脉注射2×10 ̄7个异基因脾细胞可以诱导供体特异性混合淋巴细胞反应(MLR)及细胞毒T淋巴细胞(CTL)耐受。接受异基因脾细胞门脉注射的受体鼠肝脏淋巴细胞可以非特异性地抑制MLR,但却抑制供体特异性CTL的产生,以a-H-2K ̄b单克隆抗体清除其中的供体细胞可以完全清除对供体特异性CTL产生的抑制,但只能部分地(5O%左右)清除其对MLR的非特异性抑制作用,这一结果肯定了“Veto”细胞及供体细胞中自然抑制活性在门脉耐受诱导中的作用。此外还观察到CD8 ̄+脾细胞是抑制供体特异性CTL产生的主要细胞。 相似文献
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目的:探讨肿瘤粘液糖蛋白的核心多肽MUC2诱导的抗肿瘤免疫应答。方法:测定多肽MUC2免疫后小鼠的皮肤迟发型超敏反应(DTH)和脾淋巴细胞的体外细胞毒反应。结果:MUC2可诱导小鼠的DTH;体外脾淋巴细胞对MUC2表达阳性的粘液腺癌细胞系,如人胰腺癌细胞株SW1990和人胃癌细胞株KATO-3,都具有强的细胞毒作用;抗MUC2的抗体LSB可抑制体外鼠脾细胞的细胞毒作用。结论:肿瘤相关抗原MUC2可诱导小鼠的细胞免疫应答,并可能作为一种有效的免疫原用于提高抗肿瘤免疫应答。 相似文献
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本文用3H—TdR和APAAP法研究了脐血淋巴细胞转化功能(LT)、脐血血清的特性、混合淋巴细胞反应(MLC)及T细胞亚群,结果表明脐血淋巴细胞对丝裂原的反应与正常成人外周血淋巴细胞无明显差异;脐血血清对PHA和ConA诱导的淋巴细胞转化有抑制作用;脐血之间、脐血与成人外周血之间的MLC反应均较成人外周血之间的MLC反应弱,且有显著性差异(P<0.05)。脐血细胞表型尚未成熟,脐血CD3+细胞数减低,CD4+和CD8+细胞数及其比率近似于成人,细胞数之和大于CD3+细胞数。 相似文献
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脐血与成人骨髓淋巴细胞及其亚群比较 总被引:1,自引:0,他引:1
比较脐血与骨髓T淋巴细胞、B淋巴细胞和NK细胞亚群的分布特点及血清sIL-2R和IgG水平的不同,探讨脐血移植后免疫重建延迟、GVHD及GVL效应的发生机制。应用流式细胞仪分别检测脐血及骨髓CD3+、CD3+CD5+、CD3+CD45RA+、CD3+CD45RO+、CD3+CD25+、CD19+、CD19+CD10+、CD19+CD40+、CD19+CD23+、CD3-CD16+CD56-及CD3-CD16+CD56+细胞的含量。应用双抗夹心酶联免疫吸附法(ELISA)及速率免疫散射比浊法分别检测脐血及骨髓血清中sIL-2R及IgG水平。CD3+T细胞数在脐血及骨髓中无显著差异(P>0.05)。脐血中CD3+CD45RA+、CD19+、CD19+CD10+及CD3-CD16+CD56-细胞数显著高于骨髓(P<0.05)。脐血中CD3+CD5+、CD3+CD45RO+、CD3+CD25+、CD19+CD40+、CD19+CD23+及CD3-CD16+CD56+细胞数显著低于骨髓(P<0.05)。脐血血清中sIL-2R及IgG水平显著低于骨髓(P<0.05)。脐血中成熟T细胞、成熟B细胞及成熟NK细胞亚群的细胞数显著低于骨髓,这可能是脐血移植后免疫重建延迟、GVHD发生率低及GVL效应低的原因之一。 相似文献
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During T cell development thymocyte subsets emerge in a defined order, reflective of their maturational stage. In this study we determined the timing of appearance of CD4+CD8+CD3high thymocytes during in vivo and in vitro embryonic development, and thymic reconstitution after cortisone treatment. In these models, CD4+CD8+CD3high cells followed CD4+CD8+CD3low and preceded mature CD4+CD8-CD3high/CD4-CD8+CD3high thymocytes, while cortisone resistance was first seen among CD4+CD8+CD3high cells. CD4+CD8+CD3high thymocytes were also shown to display a pattern of antigen receptor-mediated calcium influx intermediate between that induced in other CD4+CD8+ cells and mature thymocytes. These results are consistent with a precursor-progeny relationship between CD4+CD8+CD3low and CD4+CD8+CD3high thymocytes, the latter developing to mature thymocytes (Hugo, P. et al., Int. Immunol. 1991. 3: 265). 相似文献
13.
Dr. Wolfgang Saeger MD 《Endocrine pathology》2001,12(3):307-313
Immunostaining of CD markers in normal pituitary cells has been reported, but a study of these markers in pituitary adenomas
has not been done. The expression of CD 3, CD 8, CD 15, CD 20, CD 30, CD 43, CD 45R0, CD 45 R, CD 79 α, and VS-38c was investigated
in a collection of 65 pituitary adenomas of various types. CD 3 was present in 75%, CD 8 in 18.5%, CD 15 in 12.3%, CD 20 in
66.1%, CD 30 in 10.8%, CD 43 in 10.8%, CD 45 RO in 72.3%, CD 45 R in 16.9%, CD 79α in 0% and VS-38 c in 44.6%.
Densely granulated GH cell adenomas expressed CD 3, CD 20, CD 45 RO, and CD 45 R, but no other markers. Sparsely granulated
GH cell adenomas showed CD 3, CD 8, CD 20, CD 43, and CD 45 RO. Mixed GH/prolactin cell adenomas contained CD 3, CD 8, CD
20, CD 30, CD 45RO, CD 45 R, and VS-38c. Mammosomatotroph cell adenomas were positive only for CD 3, CD 8, CD 20, CD 43, and
CD 45 RO. Prolactin cell adenomas expressed CD 3, CD 8, and CD 20. ACTH cell adenomas showed CD 3, CD 15, CD 20, CD 30, CD
45 RO, CD 45 R, and VS-38c.
TSH cell adenomas contained CD 3, CD 8, CD 15, CD 20, CD 45 RO, and VS-38c.
Gonadotroph cell adenomas were positive for CD 3, CD 8, CD 20, CD 45 RO, CD 45 R, and VS-38c. Alpha-subunit-only adenomas
expressed CD 3, CD 8, CD 15, CD 20, CD 30, CD 45 RO, and VS-38c. Plurihormonal adenomas contained CD 3, CD 8, CD 20, CD 30,
CD 43, CD 45 RO, CD 45 R, and VS-38c. Oncocytic adenomas were positive for all markers except CD 45 RA and CD 79 α.
We conclude that the spectra of different adenoma types expressing CD markers varies greatly and that significant correlations
do not exist, although noninvasive adenomas appear to express CDs more frequently than invasive adenomas. We have no clear-cut
explanations for the various expressions and suggest that it may be a sign of local interactions between the immune system
and pituitary adenomas. 相似文献
14.
Caspase-8信号分子对SLE患者T细胞亚群的双向调节作用研究 总被引:1,自引:0,他引:1
目的 分析SLE患者外周血T细胞内活化Caspase-8、Caspase-3和T细胞膜上Fas、CD69以及外周血中Foxp3 CD4 CD25 调节性T细胞的表达,探讨他们在SLE患者免疫失衡中的作用.方法 用流式细胞术检测活化Caspase-8、Caspase-3和Fas、CD69以及Foxp3 CD4 CD25 Treg的表达.结果 与健康对照相比,SLE患者外周血CD3 CD4 T细胞上Fas表达显著升高(P<0.05),无论稳定期或活动期SLE患者CD3 CD4 T细胞和CD3 CD8 T细胞中活化Caspase-8的表达均显著增加(P<0.05),且稳定期和活动期SLE患者CD3 CD8 T细胞中活化Caspase-8的表达高于其在CD3 CD4 T细胞中的表达(P<0.05);但是仅活动期SLE患者T细胞内活化Caspase-3表达增加(P<0.05),同时稳定期和活动期SLE患者CD3 CD4 T细胞中活化Caspase-3的表达高于其在CD3 CD8 T细胞中的表达(P<0.05).同时SLE患者CD3 CD8 T细胞上CD69表达率升高(P<0.05),但是CD69在CD3 CD4 T细胞上的表达率与健康对照相比无显著性差异(P>0.05).SLE患者外周血中Foxp3 CD4 CD25 Treg比例显著低于健康对照(P<0.05).结论 Caspase-8介导的信号事件同时参与诱导SLE患者淋巴细胞的凋亡与活化,促使SLE患者体内免疫反应向Th2极化,同时由于SLE患者外周血中Foxp3 CD4 CD25 Treg表达降低所介导的免疫抑制效应缺陷,他们共同作用促使SLE患者外周免疫平衡障碍. 相似文献
15.
Signal transduction through CD4 receptors: stimulatory vs. inhibitory activity is regulated by CD4 proximity to the CD3/T cell receptor 总被引:26,自引:0,他引:26
J A Ledbetter C H June P S Rabinovitch A Grossmann T T Tsu J B Imboden 《European journal of immunology》1988,18(4):525-532
The binding of antibody to the CD4 molecule inhibits mobilization of cytoplasmic free calcium ([Ca2+]i) in response to CD3 cross-linking on resting T cells. Similarly, when CD3 and CD4 are independently and simultaneously cross-linked, calcium mobilization is inhibited when compared to that induced by cross-linking CD3 alone. In contrast, when anti-CD4 and anti-CD3 are cross-linked together, calcium mobilization is substantially higher than from CD3 cross-linking alone. A heteroconjugate consisting of covalently bound CD3 and CD4 monoclonal antibodies (mAb) retains the ability to mobilize [Ca2+]i in CD4 cells at protein concentrations approximately two orders of magnitude lower than the free CD3 mAb, and the activity of the heteroconjugate is inhibitable by free CD4 mAb. The CD3/CD4 heteroconjugate also shows significantly greater activity in stimulation of inositol phosphate IP1, IP2 and IP3 synthesis in T cells than the CD3 mAb alone, and again the activity is inhibited by free CD4 mAb. The activity of the CD3/CD4 heteroconjugate is not simply due to oligomerization, since CD3/CD3 or CD4/CD4 homoconjugates or homoconjugate mixtures did not show increased activity. Other heteroconjugates (CD3/CD5 and CD3/CD28) were not different than the CD3/CD3 homoconjugate in their ability to increase [Ca2+]i. Purified CD4 T cells that do not respond to CD3 mAb in solution do respond to the CD3/CD4 heteroconjugate in solution by proliferating in the presence of a CD28 mAb, with a significant fraction of CD4 cells entering the second cycle within the first three days of stimulation. The CD3/CD4 heteroconjugate co-modulates the CD3 and CD4 receptors, indicating that the heteroconjugate is not simply anchoring the T cell receptor to the T cell surface like anti-CD3 on a solid surface. These results suggest that CD4 plays an active role in signal transduction when brought into close physical proximity to the CD3/T cell receptor complex during major histocompatibility complex class II-restricted antigen presentation. 相似文献
16.
The polyclonal cytokine-induced killer (CIK) cells exhibit potent cytotoxicity against a variety of tumour cells including autologous and allogeneic acute myeloid leukaemic (AML) targets. At maturity, three lymphocyte subsets: CD3(-) CD56(+), CD3(+) CD56(-) and CD3(+) CD56(+), constitute the bulk of the CIK cell culture. The CD3(-) CD56(+) subset behaves like classical natural killer (NK) cells where cytotoxicity is potentiated by blocking the human leucocyte antigen Class I molecules in the AML targets. Both the CD3(+) CD56(+) and CD3(+) CD56(-) subsets, though known to kill autologous and allogeneic targets to a comparable degree and therefore non-major histocompatibility complex (MHC)-restricted, nevertheless require the presence of the MHC molecule on the target, which interacts with their CD3-T-cell receptor complex. Although CIK cells are often termed 'NK-like' T cells, we have demonstrated that the well-characterized NK receptors KIR, NKG2C/E, NKG2D and DNAM-1 are not involved in the process of AML recognition for the CD3(+) CD56(-) and CD3(+) CD56(+) subsets. The CD3(+) CD56(+) and CD3(+) CD56(-) subsets express a polyclonal and comparable TCRVbeta repertoire in a Gaussian distribution. The CD3(+) CD56(+) subset kills AML targets more efficiently than its CD3(+) CD56(-) counterpart because of the presence of a higher proportion of CD8(+) cells. The CD3(+) CD56(+) subset comprise more terminally differentiated late effector T cells that bear the CD27(+) CD28(-) or CD27(-) CD28(-) phenotype, with a higher granzyme A content. In comparison, the phenotype of the CD3(+) CD56(-) subset is consistent with early effector T cells that are CD27(+) CD28(+) and CD62L(+), known to be less cytotoxic but possess greater proliferative potential. 相似文献
17.
Thomassen EA Dekking EH Thompson A Franken KL Sanal O Abrahams JP van Tol MJ Koning F 《Human immunology》2006,67(8):579-588
The human T-cell receptor-CD3 complex consists of at least eight polypeptide chains; CD3gamma- and delta-dimers associate with the disulfide linked alphabeta- and zetazeta-dimers to form a functional receptor complex. The exact structure of this complex is still unknown. We now have examined the interaction between CD3gamma and CD3 in human T-cells. For this purpose, we have generated site-directed mutants of CD3gamma that were introduced in human T-cells defective in CD3gamma expression. Cell-surface and intracellular expression of the introduced CD3gamma chains was determined, as was the association with CD3delta, CD3, and the T-cell receptor. Although the introduction of wild type CD3gamma and CD3gamma (78Y-F) fully restored T-cell receptor assembly and expression, the introduction of CD3gamma (82C-S), CD3gamma (85C-S), and CD3gamma (76Q-E) all resulted in an impaired association between CD3gamma and CD3 and a lack of cell-surface expressed CD3gamma. Finally, the introduction of CD3gamma (76Q-L) and CD3gamma (78Y-A) restored the expression of TCR-CD3deltagammazeta2 complexes, although the association between CD3gamma and CD3 was impaired. These results indicate that several amino acids in CD3gamma are essential for an optimal association between CD3gamma and CD3 and the assembly of a cell-surface expressed TCR-CD3deltagammazeta2 complex. 相似文献
18.
Dichotomy of two CD8+ lymphocyte subsets in HIV infection. Depletion of CD8+ CD3- and expansion of CD8+ CD3+ subsets: consequence on the CD4/CD8 ratio.
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In order to highlight the underlying mechanism(s) of the CD8 lymphocyte expansion in the HIV infection, two distinct CD8 subsets were analysed: T CD8bright+ CD3+ with MHC-restricted activity, and non-T CD8dim+ CD3-, which performs natural killer (NK) activity. It consists of a cross-sectional study including 168 HIV-infected patients (74 CDC stage II, 48 CDC stage III and 46 CDC stage IV) compared among them and to 60 healthy individuals. We observed an expansion of CD8+ CD3+ cells which masks a depletion of CD8+ CD3-. The comparative study showed that the expansion of the CD8+ CD3+ is relatively higher than that of total CD8+ lymphocytes and that the depletion of the CD8+ CD3- subset is severe, begins early and remains constant through the HIV progression. The comparison of CD4/CD8 and CD4/CD8+ CD3+ ratios showed that the latter could possibly be a better indicator in the HIV infection. The mechanism of inverted CD4/CD8 ratio in healthy individuals was also clarified. The CD8+ CD3+, CD8+ CD3- and CD4/CD8+ CD3+ parameters would be more specific markers than total CD8 and CD4/CD8 ratio especially in therapy trials. 相似文献
19.
Expressed on the cell surface of most of NK cells and some T cells, CD161 has been shown to deliver inhibitory signal in human NK cells. To determine whether the CD161-expressing cell quantities and the cell surface expression levels of CD161 in NK and T cells were altered in systemic lupus erythematosus (SLE) patients, we analyzed the CD3, CD56 and CD161 expression patterns of peripheral blood lymphocytes by flow cytometric analysis to identify different NK and T cell subpopulations. The cell surface expression levels of CD161 were estimated by the mean florescence intensities (MFIs) of CD161. It was found that SLE patients had lower frequencies of CD161+CD56+CD3? and CD161+CD56+CD3+ cells among the lymphocyte population than normal controls, whereas the frequencies of CD161?CD56+CD3? and CD161+CD56?CD3+ cells were not statistically different between two groups. In addition, SLE patients also had decreased absolute counts of all CD161-expressing NK cells and T cells and had reduced frequencies of CD161+ cells in CD56+CD3?, CD56+CD3+ and CD56?CD3+ cell populations. Moreover, SLE patients had reduced MFIs of CD161 in CD161+CD56+CD3+ and CD161+CD56?CD3+, but not CD161+CD56+CD3?, cell populations. Our results indicated that CD161-expressing cell frequency and the CD161 expression levels were reduced in some NK and T cell subpopulations of SLE patients, suggesting possible important role of CD161 and CD161-expressing immune cells in the SLE pathogenesis. 相似文献
20.
A study on CD45 isoform expression during T-cell development and selection events in the human thymus 总被引:3,自引:0,他引:3
Fukuhara K Okumura M Shiono H Inoue M Kadota Y Miyoshi S Matsuda H 《Human immunology》2002,63(5):394-404
CD45 molecules are known to appear as various isoforms generated by alternative splicing of variable exons 4, 5, and 6, but the detailed profile of CD45 isoform expression during thymocyte development has not been revealed. We examined the CD45 isoforms expressed in the various human thymocytes' subsets defined by CD3, CD4, and CD8 expressions using RT-PCR and 4-color flow cytometry. RT-PCR study revealed that RABC, RAB, RBC, RB, and R0 isoforms were expressed in thymocytes while any of RAC, RA, or RC isoforms were not detected. RABC, RAB and RBC isoforms were expressed at CD3(-)CD4(-)CD8(-) and CD3(+)CD4(+)CD8(-) stages, but were barely detectable at CD3(-)CD4(+)CD8(+) stage. RB isoform was consistently expressed at a relatively high level at all stages. R0 isoform was expressed at a low level at CD3(-)CD4(-)CD8(-) and CD3(-)CD4(+)CD8(-) stages but upregulated at CD3(+)CD4(+)CD8(+) and CD3(+)CD4(+)CD8(-) stages. In combination with the results obtained by 4-color flow cytometric study, CD45 isoform expression on human thymocytes were determined to be RABC(+)RAB(+/-)RBC(+)RB(+)R0(+/-) at CD3(-)CD4(-)CD8(-) stage, RABC(-)RAB(-)RBC(-)RB(+)R0(+) at CD3(-)CD4(+)CD8(-) and CD3(-)CD4(+)CD8(+) stages, RABC(+/-)RAB(+)RBC(+)RB(++)R0(++) at CD3(+)CD4(+)CD8(+) stage, and RABC(+)RAB(+)RBC(+)RB(++)R0(+) at CD3(+)CD4(+)CD8(-) stage. Bcl-2 expression was upregulated between CD3(-)CD4(+)CD8(+)CD45R0(+) and CD3(+)CD4(+)CD8(+)CD45R0(+) stages. Expression of CD45R0 epitope was upregulated between CD3(-)CD4(+)CD8(+)CD69(-) and CD3(+)CD4(+)CD8(+)CD69(+) stages while CD45RA epitope expression was unchanged. Thus, when thymocytes are positively selected, CD45R0 isoform expression seems to be upregulated while CD45RABC isoform expression stays at a very low level. In summary, various isoforms of CD45 were shown to be tightly regulated during thymocyte development and through the selection process. 相似文献