Human interleukin-2 promotes proliferation of activated B cells via surface receptors similar to those of activated T cells

Human interleukin-2 (IL-2) is a glycoprotein of relative molecular mass (Mr) 15,000, which is released by T lymphocytes on stimulation with antigen or mitogen and functions as a T-cell growth factor (TCGF) by inducing proliferation of activated T cells. It is generally accepted that resting or activated B cells do not respond directly to IL-2 but require for their proliferation other T-cell-derived lymphokines usually referred to as B-cell growth factors (BCGFs). Recently, however, a monoclonal antibody reacting with the IL-2 receptor molecules expressed by activated T cells (anti-Tac) was shown to react also with certain B tumour cells; in addition, murine B cells proliferate in response to pure human IL-2. We now show that recombinant IL-2, derived from Escherichia coli expressing the human gene, is able to promote strong proliferation of human B cells activated with protein-A-rich Staphylococcus aureus Cowans strain I. Moreover, we demonstrate that the anti-Tac antibody also reacts with S. aureus-activated normal B cells and inhibits sharply the proliferative response of such cells to IL-2. Finally, immunoprecipitation experiments reveal that anti-Tac defines similar molecules on activated T and B cells.     

Induction and effector functions of T(H)17 cells

T helper (T(H)) cells constitute an important arm of the adaptive immune system because they coordinate defence against specific pathogens, and their unique cytokines and effector functions mediate different types of tissue inflammation. The recently discovered T(H)17 cells, the third subset of effector T helper cells, have been the subject of intense research aimed at understanding their role in immunity and disease. Here we review emerging data suggesting that T(H)17 cells have an important role in host defence against specific pathogens and are potent inducers of autoimmunity and tissue inflammation. In addition, the differentiation factors responsible for their generation have revealed an interesting reciprocal relationship with regulatory T (T(reg)) cells, which prevent tissue inflammation and mediate self-tolerance.     

Anti-TOSO antibody treatment promotes T cell activation-induced cell death （AICD） in vitro and in vivo

T cell activation-induced cell death （AICD）, that involves the induction of Fas-mediated apoptosis, is very important for the maintenance of immune homeosta- sis. TOSO was firstly described as an inhibitor of Fas- mediated apoptosis and overexpressed in chronic lymphocytic leukemia. Recently, TOSO was identified as IgM FcR. In this study, we produced anti-TOSO monoclonal antibody （mAb） that could block the binding of IgM to TOSO and found that T cell apoptosis is negatively cor- related with TOSO expression during T cell activation. Treatment of activated T cells with anti-TOSO blocking mAb promoted T cell AICD in in vitro AICD model, and treatment of xenogeneic-GVHD mice with the antibody also increased the sensitivity of activated T cells to Fas- induced apoptosis, which was accompanied by reduction of c-FLIPL expression and up-regulation of AP-1 complex. In summary, our data indicate the anti-apoptotic effect of TOSO in T cell AICD and open up new therapeutic prospects for the treatment of hematologic malignancies and immune disorders.     

人翻译延伸因子eEF1A1促进肺癌细胞H1299对紫杉醇和阿霉素药物耐受的研究

在已知人翻译延伸因子eEF1A的多功能性和与细胞存活相关的基础上,本文进一步研究eEF1A的变体蛋白eEF1A1对癌细胞耐药性的影响.eEF1A1基因的蛋白质编码区经过克隆,并瞬时转染了人肺癌细胞H1299,在确定eEF1A1蛋白的胞内表达后,采用MTT法测定高表达eEF1A1的H1299细胞对抗癌药物紫杉醇和阿霉素的耐受.相对于对照细胞,eEF1A1的高表达可显著提高H1299细胞对阿霉素和紫杉醇的耐受性.通过耐药性测试揭示出eEF1A可能参与肿瘤发生的潜在功能.     

Regulated expression and binding of three VLA (beta 1) integrin receptors on T cells

Regulated adhesion of T cells to extracellular matrix (ECM) proteins is likely to be essential in T cell migration. Constitutive binding of various other cell types to ECM components is mediated by members of the VLA (very late antigen) subfamily of integrins. We describe here the regulated binding of resting CD4+ human T cells to ECM through three VLA integrins: VLA-4 and VLA-5 binding to fibronectin (FN), and a novel pathway of VLA-6 binding to laminin (LN). Binding to ECM is regulated in two ways. First, unlike other VLA-mediated interactions, VLA binding activity of the T cells is rapidly and dramatically augmented with cell activation without change in level of expression of the VLA molecules. Second, binding is regulated with T-cell differentiation; memory T cells express three- to four-fold more VLA-4, VLA-5, and VLA-6 than do naive cells, and bind more efficiently through them to FN and LN.     

IL-21 initiates an alternative pathway to induce proinflammatory T(H)17 cells

On activation, naive T cells differentiate into effector T-cell subsets with specific cytokine phenotypes and specialized effector functions. Recently a subset of T cells, distinct from T helper (T(H))1 and T(H)2 cells, producing interleukin (IL)-17 (T(H)17) was defined and seems to have a crucial role in mediating autoimmunity and inducing tissue inflammation. We and others have shown that transforming growth factor (TGF)-beta and IL-6 together induce the differentiation of T(H)17 cells, in which IL-6 has a pivotal function in dictating whether T cells differentiate into Foxp3+ regulatory T cells (T(reg) cells) or T(H)17 cells. Whereas TGF-beta induces Foxp3 and generates T(reg) cells, IL-6 inhibits the generation of T(reg) cells and induces the production of IL-17, suggesting a reciprocal developmental pathway for T(H)17 and T(reg) cells. Here we show that IL-6-deficient (Il6-/-) mice do not develop a T(H)17 response and their peripheral repertoire is dominated by Foxp3+ T(reg) cells. However, deletion of T(reg) cells leads to the reappearance of T(H)17 cells in Il6-/- mice, suggesting an additional pathway by which T(H)17 cells might be generated in vivo. We show that an IL-2 cytokine family member, IL-21, cooperates with TGF-beta to induce T(H)17 cells in naive Il6-/- T cells and that IL-21-receptor-deficient T cells are defective in generating a T(H)17 response.     

半群BR(T,θ)与半群T的结构

论述了一个半群T的关于同态θ的Bruck—Reilly扩张半群BR(T，θ)与半群T在结构性质上的关系。     

关于特征函数T(r,f)与T(r,1/f)的关系

本文研究亚纯函数f(z)与1/f(z)的特征函数T(r,f)与T(r,1/f)之间的关系。由Jensen公式推导出了它们的关系式,从而证明了特征函数T(r,f)与T(r,1/f)之间只相差一个常数。     

Ba_3Ti_5Nb_(6-x)TaxO_(28)陶瓷的结构与介电性能

采用传统的固相合成法制备Ba3Ti5Nb6-xTaxO28(0≤x≤0.67)微波介质陶瓷,研究了Ta对Ba3Ti5Nb6O28陶瓷结构与微波介电性能的影响.随Ta含量的增加,Ba3Ti5Nb6-xTaxO28陶瓷先为Ba3Ti5Nb6O28单相;当x增大到0.5时,则出现了第二相Ba3Ti4Nb4O21.随Ta含量增加,Ba3Ti5Nb6-xTaxO28陶瓷的介电常数变化较小,Qf值先明显升高后下降,而谐振频率温度系数τf逐渐增大.x=0.16时,获得了介电性能优异的Ba3Ti5Nb6-xTaxO28陶瓷,介电性能为:ε=37.9,Qf=2.8137×104GHz,τf=-6.0×10-6℃-1.     

t(n)分布及其渐近性质

t(n)分布是数理统计中的一个非常重要的分布,本文详细地讨论了它的性质,并作出了归纳和证明,特别是分别利用Stirling公式、定积分公式以及概率论中的收敛性从不同的角度证明了它的著名的渐近性质,并指出了t(n)分布和标准正态分布之间存在的差异。     

T(d,n)~4He反应的中子能谱的测量和模拟计算

本文描述用飞行时间谱仪对T(d,n)~4He反应的α关联中子能谱和角分布的测量,以及介绍对这些中子能谱的蒙特卡罗模拟。在计算中考虑了氘在氚-钛靶的多次散射。对发射中子谱自寺和关联中子平均能量的计算结果分别与Pavlik等人的计算结果和我们的实验结果很好地符合。     

(T,N)-蕴涵及其基本性质

模糊蕴涵在模糊逻辑和近似推理领域中发挥着非常重要的作用。 不同的构造方法可以生成不同的模糊蕴涵, 其中常见的模糊蕴涵类有(S,N)-蕴涵、 R-蕴涵、 QL-蕴涵和Yager蕴涵等。 从经典逻辑中的重言式p→q≡(p∧q)出发, 在模糊逻辑中研究由三角模T和模糊否定N按上述方式生成的模糊蕴涵, 称为(T,N)-蕴涵, 进而研究(T,N)-蕴涵的一些基本性质, 包括输入律与分配性等。 最后讨论(T,N)-蕴涵与 f-蕴涵、 g-蕴涵、(S,N)-蕴涵和R-蕴涵间的关系。     

关于W（T）的不可达点和端点

设T是作用在Hilbert空间H上的有界线性算子,W（T）是T的数值域,W（T）是W（T）的闭包,W（T）是W（T）的边界。讨论并给出了W（T）／W（T）中的点的一些性质。     

Skin infection generates non-migratory memory CD8+ T(RM) cells providing global skin immunity

Protective T-cell memory has long been thought to reside in blood and lymph nodes, but recently the concept of immune memory in peripheral tissues mediated by resident memory T (T(RM)) cells has been proposed. Here we show in mice that localized vaccinia virus (VACV) skin infection generates long-lived non-recirculating CD8(+) skin T(RM) cells that reside within the entire skin. These skin T(RM) cells are potent effector cells, and are superior to circulating central memory T (T(CM)) cells at providing rapid long-term protection against cutaneous re-infection. We find that CD8(+) T cells are rapidly recruited to skin after acute VACV infection. CD8(+) T-cell recruitment to skin is independent of CD4(+) T cells and interferon-γ, but requires the expression of E- and P-selectin ligands by CD8(+) T cells. Using parabiotic mice, we further show that circulating CD8(+) T(CM) and CD8(+) skin T(RM) cells are both generated after skin infection; however, CD8(+) T(CM) cells recirculate between blood and lymph nodes whereas T(RM) cells remain in the skin. Cutaneous CD8(+) T(RM) cells produce effector cytokines and persist for at least 6 months after infection. Mice with CD8(+) skin T(RM) cells rapidly cleared a subsequent re-infection with VACV whereas mice with circulating T(CM) but no skin T(RM) cells showed greatly impaired viral clearance, indicating that T(RM) cells provide superior protection. Finally, we show that T(RM) cells generated as a result of localized VACV skin infection reside not only in the site of infection, but also populate the entire skin surface and remain present for many months. Repeated re-infections lead to progressive accumulation of highly protective T(RM) cells in non-involved skin. These findings have important implications for our understanding of protective immune memory at epithelial interfaces with the environment, and suggest novel strategies for vaccines that protect against tissue tropic organisms.     

广义Г-环上模的Morita结构及其应用

引进广义Г-环上模的Morita结构概念,建立模的Morita结构理论及其构造M,应用它们给出左、右Artin单广义Г-环结构定理的证明.     

广义逆A_(T,S)~(2)的表示与计算

比较系统的总结了AT,S(2)的各种表示,与此同时,给出AT,S(2)的三个新的表达式,AT,S(2)=[E1GA E2]-1[E10]G或AT,S(2)=G(F1 0)-1(AGF1 F2)以及AT,S(2)=-1/β0((GA)s-1+βs-1(GA)s-2+…+β2(GA)+β1In)G=-1/β0G((AG)s-1+βs-1(AG)s-2+…+β2(AG)+β1In)利用前两种表达式,我们给出AT,S(2)逆的Gauss-Jordan消去法的求法.     

CXW-180-JXD28型吸油烟机振动和噪声测试分析

根据国家标准,在半自由声场的振动和噪声实验条件下,对CXW-180-JXD28型吸油烟机进行了噪声和振动测试,分析相关测试数据,找出主要振动和噪声源,并探讨了改进措施.该机型的主要振动和噪声源为离心风机和箱体,可以通过合理选型、优化风机结构、控制机械噪声等措施减少噪声与振动的产生.