食管癌间质反应及T淋巴细胞亚群分布规律的研究

用单克隆抗体作碱性磷酸酶—抗碱性磷酸酶(简称APAAP)复合物免疫酶染色,定量分析食管鳞癌组织中浸润的T淋巴细胞及其亚群,同时观察炎细胞反应程度。结果发现,OKT_1(简称T_1)细胞的浸润密度随癌分化程度的降低而减少,分化差的癌组织内OKT_4(简称T_4)细胞减少,OKT_8(简称T_8)细胞相对增多,致T_4/T_8比值下降。间质淋巴样细胞多者,T_1和T_4细胞也相对较多,但T_8细胞及T_4/T_8比值与炎细胞反应程度无明显关系。提示不能以局部淋巴样细胞或T淋巴细胞的单纯计数和计量来代替检测T_4/T_8比值。     

用武系列单克隆抗体检测健康成人外周血淋巴细胞亚群

本文应用国产自制武系列抗人淋巴细胞单克隆抗体与进口OKT系列对比检测103例健康成人外周血T淋巴细胞的正常值。经免疫荧光法检查,Wu71(抗人金T)与外周血单个核细胞反应,Wu167(抗人辅助性T亚群)和Wu448(抗人抑制性T亚群)分别与43.8±9.0％(30％～61％)和31.3±7.0％(20％～48％)外周血单个核细胞反应。Wu167/Wu448之值为1.48±0.5(0.88～2.48)。本文结果还证实上述结果与相应抗人全T单抗(OKT_3),OKT_4,OKT_8的测定值相此无显著性差别。不同性别和不同年龄组的细胞及亚群测定值统计表明:T细胞总数随年龄增长有下降趋势,以男性中老年组与青年组之间差异较显著。T_4受年龄影响较小而性别之间差异较大,女性的T_4及T4/T8明显高于男性。T_8除男性老年组明显低于男性青年组外,其余均无明显差异。     

人的活化T细胞出现的T_4~+T_6~+双标记现象

OKT系列单克隆抗体的产生,促进了人T细胞亚类的划分。最初的报道认为,人的外周血T细胞可分为OKT_4~+(T_4~+)和OKT_8~+(T_8~+)细胞两个亚类,分别占T细胞总数的55～65%和30～40%。最近有报道指出,人的末梢血中存在少量的T_4~+T_8~+双标记细胞,在体外活化的T细胞,可以暂时     

慢性乙型肝炎患者外周血T细胞亚群及T_4/T_8双标志细胞的初步研究

本文应用抗人T细胞单克隆抗体借助葡萄球菌-羊红细胞直接双花环法研究了11例慢性乙型肝炎患者外周血T细胞亚群.结果发现.慢性乙型肝炎患者外周血T_4~+细胞(辅助/诱导T细胞)数在正常范围;T_8~+细胞抑制/细胞毒T细胞数与正常对照比较明显增加;T_4/T_8比值与正常对照比较明显降低.此外。在慢性乙型肝炎患者外周血中发现有较多的可同时表达T_4和T_8抗原的细胞。其功能和意义尚待进一步研究.     

癫痫患者淋巴细胞亚群和NK细胞活性的研究

本文以单克隆抗体间接免疫荧光法检测了58例癫痫患者和22例同龄健康献血者的外周血T细胞亚群、B细胞单核巨噬细胞.用~(s1)Cr释放法测定外周血单个核细胞(PBMC)中的自然杀伤(NK)细胞活性。结果表明癫痫患者T_3和T_4细胞百分率均低于对照组,T_8细胞百分率增高,T_4/T_8比值显若降低,B细胞和单核巨噬细胞未见明显改变.NK细胞活性降低。提示本病存在细胞免疫功能异常。     

茶碱敏感和茶碱抵抗T细胞及自身花T细胞的单克隆抗体鉴定

茶碱敏感T细胞(Ts)和茶碱抵抗T细胞(T_R)已被许多实验证明分别具有抑制和增强免疫反应的作用。自身玫瑰花形成T细胞(Tarf)的功能因实验条件不同而不同。它们是外周血液中互不相同的T细胞亚群。以T细胞形成玫瑰花的功能而划分的T细胞亚群,其表面标志如何,是一个非常有意义的问题。本文用几种白细胞单克隆抗体对上述三种T细胞进行了检查,发现T_(44)(相当于OKT_4),阳性细胞在Ts,T_R及Tarf中分別为17.74％,51.87％和37.9％;Leu2b(相当于OKT_8)阳性细胞在Ts、T_R、Tarf中分别为34.83％,     

以OKT单克隆抗体研究胃癌及系统性红斑狼疮(SLE)患者的外周血 T 淋巴细胞亚群

以鼠抗人 OKT_3、OKT_4、OKT _8三种单克隆抗体检测37例进展型胃癌及23例SLE 患者的外周血中 T 细胞及其亚群细胞的百分值,并计算 OKT_4/OKT_8细胞的百分比值。结果发现胃癌组表现为 OKT_4细胞的降低,OKT_8细胞的增高,OKT_4/OKT_8比值降低,仅为1.2±0.4。其中晚期胃癌组30例中此改变尤为突出,OKT_4/OKT_8比值仅为1.12±0.3(与正常对照2.1±0.5相比,P<0.001)。活动型 SLE 患者正与胃癌组相反,表现为 OKT_8细胞的降低,仅为18.5±4.1%,因而 OKT_4/OKT_8比值增高为3.0±0.5。随着治疗后病情好转,OKT_8细胞恢复正常,而 OKT_4细胞降低(可能与肾上腺皮质激素有关),因而 OKT_4/OKT_8比值反有降低。     

人对白细胞间介素-2的反应及其产生的细胞基础 用单克降抗体鉴定的自身玫瑰花形成细胞的作用

作者用自身玫瑰花形成T细胞(Tar)和花生凝集素(PNA)将T细胞亚群(T_4~+与T_8~+)进一步分成不同的组份,分析了这些不同组份产生白细胞间介素-2(IL-2)和对其反应的情况,同时提及了对IL-1的反应。用梯度离心及E玫瑰花法从健康人外周血中分离获取T细胞,以OKT_4和OKT_8单克隆抗体加补体的阴性选择法纯化分离T_4~+和     

T淋巴细胞克隆技术

现代免疫学的发展越来越表明T淋巴细胞是高度异质性细胞群。Blue等用双色荧光标记检测发现,正常人周围血中有3%的T细胞可同时表达T_4及T_8抗原。Krensky等观察到了有T_4~+表型的细胞毒T淋巴细胞(CTL)。这种细胞的杀伤作用不被OKT_8单克隆抗体(McAb)所阻断。     

19例原发性干燥综合症病人T细胞亚群测析

本文用单克隆抗体间接免疫荧光法检测了19例原发性干燥综合症(PSS)、7例系统性红斑狼疮(SLE)病人和16例正常人的外周血T细胞亚群。结果表明,PSS患者T_3~ 、T_4~ 、T_8~ 细胞及T_4/T_8比值与正常人无明显差别,而与SLE病人有明显不同。提示PSS病人外周血T细胞亚群数量的变化不能完全反映其功能情况,也不反映受累组织内淋巴细胞的组成。     

T cell homeostasis: keeping useful T cells alive and live T cells useful

It has become clear that the regulation of T cell numbers is under peripheral homeostatic control. However, the rules for homeostasis vary with the T cells' differentiation state and the overall T cell number in the animal. Furthermore, homeostatic pressures can cause unexpected changes in T cell differentiation and function which might promote or dampen T cell reactivity. In this review, we focus on the role of peptide/MHC and cytokine interactions in regulating the size and composition of the T cell pool.     

Designer T cells by T cell receptor replacement

T cell receptor (TCR) gene transfer is a convenient method to produce antigen-specific T cells for adoptive therapy. However, the expression of two TCR in T cells could impair their function or cause unwanted effects by mixed TCR heterodimers. With five different TCR and four different T cells, either mouse or human, we show that some TCR are strong--in terms of cell surface expression--and replace weak TCR on the cell surface, resulting in exchange of antigen specificity. Two strong TCR are co-expressed. A mouse TCR replaces human TCR on human T cells. Even though it is still poorly understood why some TCRalpha/beta combinations are preferentially expressed on T cells, our data suggest that, in the future, designer T cells with exclusive tumor reactivity can be generated by T cell engineering.     

Inhibition of T lymphocyte heparanase by heparin prevents T cell migration and T cell-mediated immunity

Previously we reported that activated T lymphocytes express a heparanase enzyme that degrades the heparan sulfate moiety of the proteoglycan of the extracellular matrix (ECM). Expression of the heparanase enzyme was found to be associated with the ability of activated T lymphocytes to penetrate blood vessel walls and accumulate in target organs. We recently found that relatively low doses of heparin administered to mice or rats inhibited T cell-mediated immune reactions. In the present study we investigated the effects in vitro and in vivo of the heparanase inhibitor, heparin, on the expression of T lymphocyte heparanase and on the ability of T lymphocytes to mediate a delayed-type hypersensitivity (DTH) reaction. We found that heparanase was induced by immunizing mice with antigen in vivo or by activating T lymphocytes with concanavalin A in vitro. Relatively low doses of heparin administered once daily in vivo (5 micrograms) or present in vitro (0.1 microgram/ml) inhibited the expression of heparanase induced by immunization or by concanavalin A incubation. Higher or lower doses of heparin did not have these effects. The same doses of heparin that inhibited expression of heparanase also inhibited the ability of the lymph node cells to migrate to a site of antigen and adoptively produce a DTH reaction. These findings suggest that modulation of cell-mediated immune reactions may be achieved by relatively low doses of heparin which inhibit expression of T lymphocyte heparanase.     

T cytotoxic 1 and T cytotoxic 2 CD8 T cells both inhibit IgE responses

BACKGROUND: It is well recognized that CD8 T cells inhibit IgE responses. In this study, we investigated the mechanism of CD8 T cell-mediated IgE suppression by comparing the capacity of T cytotoxic 1 (Tc1) and T cytotoxic 2 (Tc2) CD8 T cells to inhibit IgE responses to ovalbumin (OVA). METHODS: Tc1 and Tc2 CD8 T cells were generated from OVA(257-264)-specific Vbeta5.2 T cell receptor (TcR) transgenic mice by stimulation with anti-CD3 and anti-CD28 under Tc1 and Tc2 polarizing conditions. Tc1 and Tc2 Vbeta5.2 TcR CD8 T cells (10(6)) were adoptively transferred to syngeneic mice, and following immunization with 100 micro of OVA/alum, serum IgE antibodies were measured by passive cutaneous anaphylaxis and expressed as the highest dilution that gave a detectable skin response. RESULTS: Both Tc1 and Tc2 CD8 T cells from OT-I mice inhibited IgE. CONCLUSION: Both Tc1 and Tc2 CD8 T cells promote Th1 immunity and inhibit IgE responses. This process appears to be independent of CD8 T cell-derived IFN-gamma, as both Tc2 (IFN-gamma-) and Tc1 (IFN-gamma+) CD8 T cells inhibited IgE.     

T1-selective diffusion weighted fMRI at 1.5T

Apparent diffusion coefficients (ADC) of protons contributing to the functional signal can be determined from diffusion weighted functional magnetic resonance imaging (MRI) studies. An earlier study indicated that ADCs calculated from the functional signal of an activated primary sensorimotor cortex are large, and consistent with a CSF or intravascular contribution to the functional signal. We have added inversion recovery pulses to isotropic diffusion weighted imaging to null CSF protons selectively within the imaging slice, or to null the outer volume blood flowing into the imaging slice. With the use of gradient recalled diffusion weighted echo-planar imaging at low gradient b factors, and without the use of inversion pulses, the ADCs x 10(3) in mm2/s (+/- SD) from the functional signal were 6.81 +/- 1.19. These ADCs were significantly higher than resting primary sensorimotor cortex ADCs of 2.26 +/- 1.49, measured at the same b factors. When CSF nulling was applied, the functional signal ADCs remained high. Application of inflow nulling decreased the functional signal to such a small value, that ADCs estimated from these functional signals were not assessed. The results are consistent with an intravascular contribution to the functional signal and to its large ADC.     

REDIRECTING T LYMPHOCYTE SPECIFICITY USING T CELL RECEPTOR GENES

Redirecting T cells by transferring T cell receptor (TCR) genes from tumor-associated antigen (TAA)-reactive T cell clones into human peripheral blood lymphocytes (PBL) has therapeutic potential for the treatment of diseases, including cancer. T cell specificity can be altered using retroviruses encoding TCR &#102 and TCR &#103 chain genes, or chimeric immunoglobulin (cIg) genes containing signaling domains of CD3 &#145 or Fc &#108 RI- &#110. This review evaluates recent studies using TCRs and cIgs to redirect T cell specificity and discusses some of the technical and biological hurdles that need to be addressed before these approaches can be successfully used to treat patients.