正常人B细胞产生B细胞生长因子

抗原或表面免疫球蛋白交键因子,例如抗-μ或金黄色葡萄球菌Cowan I(SAC)能激活B细胞。用抗-μ激活B细胞时,细胞的增殖需要B细胞生长因子(BCGF),细胞的分化需要B细胞分化因子(BCDF)。但是如用SAC激活人体休止期B细胞时,B细胞不需要外源性BCGF,只要与BCDF反应后就可以产生免疫球蛋白(Ig)。这提示SAC能起BCGF样作用或SAC能促使B细胞产生BCGF样的活性。已证明人恶性B细胞瘤系和/或EB病毒转化的B细胞能产生促B     

B7家族的新成员—B7-H1、B7-H2、B7-H3、B7-DC

T细胞的活化需要TCR与抗原肽-MHC的第一信号，以及共刺激因子的第二信号系统。B7家族是重要的共刺激分子，属于免疫球蛋白家族。除B7-1和B7-2外，近几年又发现了B7家族的新成员——B7-H1、B7-H2、B7-H3、B7-DC等，与T、B细胞的活化及免疫应答等有关。深入研究B7家族成员的结构和作用机制，有助于T、B细胞活化机制以及免疫耐受、肿瘤免疫研究的深入和发展。     

B细胞系抑制性淋巴细胞——抑制B细胞

B细胞抑制的现象学抑制B细胞在各种器官中的分布在体内能抑制抗体产生的抑制B细胞存在于骨髓、脾脏和淋巴结,胸腺中无抑制B细胞。致敏豚鼠和小鼠的脾脏、淋巴结中存在能够特异地抑制迟发型超敏反应的抑制B细胞。在肿瘤诱导下,脾脏可以出现能非特异地抑制免疫反应的抑制B细胞。等人研究了在体外能抑制抗体产生的抑制B细胞在正常小鼠、B鼠(切除胸腺,再予以致死性照射,然后注射骨髓使之恢复的小鼠)以及裸鼠淋巴样组织中的分布,证实了B鼠和裸鼠的骨髓细胞和正常     

B细胞生长因子

<正> 1971年Dutton首先发现T细胞可溶性因子与B细胞活化有关,迄今发现除了白细胞间介素-2(IL-2)以外,至少有三种T细胞分泌的因子能影响B细胞的增殖和/或分化,将其统称为B细胞刺激因子(BSF),依它们的功能特性可分成三大类:1.与活化的B细胞增殖有关的因子(BCGF I或BSF-p1);2.与     

B Cell Deficiencies

Genetics of IgA deficiency and CVID;X-linked agammaglobulinemia;     

载脂蛋白B研究进展

人载脂蛋白Ｂ有ａｐｏＢ－１００和ａｐｏＢ－４８两种类型。ａｐｏＢ－１００天然状态下呈网状包绕在ＬＤＬ颗粒表面。肠粘膜细胞内存在有特殊ａｐｏＢｍＲＮＡ编辑机制，它将ａｐｏＢｍＲＮＡ上第２１５３个密码子改编为终止密码子，导致ａｐｏＢ－４８生成。ａｐｏＢ多种基因突变引起ＦＨＬ和ＦＤＡ两种遗传性缺陷。     

B细胞生长因子

自从发现在抗体产生过程中T-B细胞相互作用以来,关于T细胞调节B细胞对抗原产生免疫应答的作用机制已经进行了广泛的研究.大量实验证明T细胞的辅助功能是通过释放可溶性物质介导的.至今,已报告的由T细胞产生的可溶性物质有多种,被统称为B细胞刺激因子(BSF).各种BSF的性质和功能不尽相同.本文试述T细胞产生的具有诱导B细胞增殖活性的因子,即B细胞生长因子(BCGF)如下.     

B细胞淋巴因子

免疫系统在对抗原刺激应答时,B细胞克隆扩增及分化的特异性越来越多地归因于宿主的可溶性因子。1985年TadamitsuKishimoto在一篇文章中讨论了BCGF-Ⅰ、BCGF-Ⅱ、BCDFs-γ、μ,BCDF、BRF、BMF和BSF等关于B细胞生长、分化、增殖、成熟和刺激因子。在抗原与淋巴细胞受体结合所触发的反应中,信号不仅仅起放大作用,淋巴因子涉及了从B细胞早期激活到最终分化成抗体生     

载脂蛋白B研究进展

载脂蛋白B(apolipoprotein B,ApoB)在脂类代谢、胆固醇的运输中起关键性的作用,其在心血管疾病、家族性β脂蛋白血症、肥胖和胆囊疾病的研究中尤为重要。本文对ApoB独特的基因结构、表达模式及其多态性与疾病关系的研究进展进行了综述。     

New alleles in the B44 family including B*44022, B*44032, B*4411, B*4420, B*4421, B*4424, and B*8301

Seven new HLA-B locus alleles have been described. B*44022 and B*44032 are silent substitutions altering known alleles. B*4411 carries a unique Bw4-like epitope. B*4420, B*4421, and B*4424 carry new combinations of motifs previously observed in other alleles. B*8301 appears to be the result of the replacement of exon 2 from B*4402 with exon 2 from B*5603.     

Unique B cell responses in B cell-dependent and B cell-independent EAE

Previous studies characterized B cell-dependent and B cell-independent models of experimental autoimmune encephalomyelitis (EAE) in C57BL/6 mice. To further characterize the B cell response generated in these two models, the serum antibody response and the B cell surface immunoglobulin (Ig) repertoire were analyzed following immunization of wild-type C57BL/6 mice with either recombinant myelin oligodendrocyte glycoprotein (MOG; B cell-dependent EAE) or the encephalitogenic MOG(35-55) peptide (B cell-independent EAE). Plasma ELISA revealed responses to unique linear epitopes of MOG following immunization with recombinant MOG that were absent in MOG(35-55)-immunized animals. B cell repertoire analysis by RT-PCR identified a unique response restricted to 7183 Ig heavy chain variable gene family in mice immunized with recombinant MOG that was not observed in MOG(35-55)-immunized mice. These insights could aid in the identification of the relevant B cell populations important to the pathogenesis of B cell-dependent EAE and in the mechanisms by which these B cell populations contribute to disease.     

Biomedical applications of 10B and 11B NMR

This review focuses mainly on the detection and investigation of molecules used for boron neutron capture therapy (BNCT) by 10B and 11B NMR. In this binary radiation treatment, boron-containing molecules (also called 'BNCT agents') enriched in the 10B isotope, are targeted to the tumor, and irradiated with thermal or epithermal neutrons. Capture of these neutrons by 10B nuclei generates cell-damaging radiation, confined to single cell dimensions. NMR research efforts have primarily been applied in two directions: first, to investigate the metabolism and pharmaco-kinetics of BNCT agents in-vivo, and second, to use localized NMR spectroscopy and/or MRI for non-invasive mapping of the administered molecules in treated animals or patients. While the first goal can be pursued using 11B NMR for natural-abundance samples (80% 11B / 20% 10B), molecules used in the actual treatment are > 95% enriched in 10B, and must therefore be detected by 10B NMR. Both 10B (spin 3) and 11B (spin 3/2) are quadrupolar nuclei, and their typical relaxation times, in common BNCT agents in biological environments, are rather short. This poses some technical challenges, particularly for MRI, which will be reviewed, along with possible solutions. The first attempts at 11B NMR and MRI detection of BNCT agents in biological tissue were conducted over a decade ago. Since then, results from 11B MRI in laboratory animals and in humans have been reported, and 11B NMR spectroscopy provided interesting and unique information about the metabolism of some BNCT agents in cultured cells. 10B NMR was applied either 'indirectly' (in double-resonance experiments involving coupled protons), but also by direct 10B MRI in mice. However, no results involving the NMR detection of 10B-enriched compounds in treated patients have been reported yet.     

The modulation of B7.2 and B7.1 on B cells by immunosuppressive agents.

Several recent studies demonstrate that B7.2, but not B7.1, play an important role in allergic inflammation and IgE production. Agents that down-regulate B7.2 may therefore be of benefit for the treatment of Th2-driven allergic diseases. Our current study was carried out to investigate the effect of immunosuppressive agents, cyclosporin A (CsA) and dexamethasone, on B7.2 and B7.1 expression on B cells stimulated with the superantigen, toxic shock syndrome toxin-1 (TSST-1). The analysis of B7.2 and B7.1 on the same cells by flow cytometry demonstrated that TSST-1 up-regulated B7.2+B7.1- but not B7.1+B7.2- on B cells in a dose-dependent fashion. CsA and dexamethasone significantly down-regulated B7.2+B7.1- but up-regulated B7.2-B7.1+ B cells in the presence or absence of TSST-1 (100 ng/ml). Interestingly, the combination of CsA and dexamethasone was much more potent in the inhibition of B7.2 expression than either of these agents alone. As CD40 is known to up-regulate B7.2 expression on B cells, the mechanism of B7.2 down-regulation by CsA and dexamethasone was further studied by investigating the effect of these agents on CD40 expression on B cells. TSST-1 significantly increased CD40 expression on B cells. However, the addition of CsA or dexamethasone significantly down-regulated CD40 expression. Anti-CD40 MoAb significantly reversed the effects of CsA or dexamethasone on B7.2 and B7.1 expression, suggesting that T cell engagement of CD40 plays a role in the mechanisms by which CsA and dexamethasone acts on B cells. These data demonstrate the modulatory effect of CsA and dexamethasone on B7.2 and B7.1 expression on B cells and the potential role of CD40 in mediating this effect.     

Monoclonal antibodies for fumonisins B1, B2 and B3

There has been only one report of fumonisin antibodies produced from a fumonisin-bovine serum albumin (BSA) immunogen in the past. Other, more exoteric, carriers, such as cholera toxin and keyhole limpet hemocyanin, have also been used. The resulting antibodies have a wide range of sensitivity and selectivity for the most common fumonisins B₁, B₂ and B₃. We report on fumonisin monoclonal antibodies produced in typical fashion from an immunogen consisting of FB₁ conjugated to BSA through its terminal amino group. These antibodies have excellent cross-reactivity with the three main fumonisins: FB₁, 100%, FB₂, 94%, and FB₃, 72%, adequate sensitivity with an IC₅₀ of 430 ng/mL for FB₁, and show excellent correlation between ELISA and total fumonisins as determined by HPLC, with a slope of 0.985 and an r² of 0.987.     

Three newly identified HLA-B alleles: B*5124, B*5306, B*5307 and confirmation of B*0809 and B*5606

Five HLA-B sequences are described which have been detected as irregular patterns during routine molecular typing. Sequencing of HLA-B exon 2 and 3, both heterozygous and after group specific amplification, revealed three new HLA-B alleles: B*5124, B*5306 and B*5307, whereas the sequences of B*0809 and B*5606 were confirmed. Serological typing showed that B*0809 is expressed as a regular B8, B*5124 as a regular B51, B*5306 as a B51/B53-like variant and B*5606 as a B"blank"-Bw6.     

Selection of B cell clones and memory B cells.

During a humoral immune response, a variety of histological, cellular, and molecular changes occur within the immune system. In this review, we would like to summarize and integrate these changes with a view toward gaining insight into the process of clonal selection. We describe here how antigen receptor number limits the sensitivity of a B cell to transduce a signal in response to antigen. We have also seen that this limitation can be compensated for by expressing a higher affinity receptor for antigen. These data suggest that the down regulation of antigen binding receptors in germinal center cells might be designed to exploit anticipated increases in affinity that result from somatic hypermutation in these tissues. This hypothesis is consistent with observed biological changes that occur during an immune response and has bearing on both the mechanism of affinity maturation and generation of immunologic memory.