云南怒族八种红细胞血型抗原调查分析

目的 :了解云南怒族ABO、Rh、MN、P、GPC、GPA、KeLL、Wrb血型系统抗原分布情况 ,为解决临床输血及人类学、遗传学、分子生物学提供理论依据。方法 :在怒族自然村采用随机抽样调查128人 ,进行血清学检测定型的方法。结果 :云南怒族ABO血型系统中表现型A>O>B>AB ;基因频率r>p>q。Rh血型系统中Rh( -D)阴性率占4 69 % ,d基因频率为0 2165 ,分布较高于我国各民族(除新疆维吾尔族外) ,该民族表现型CCDee居多 ,占31 25% ,其分布特征为CCDee>CcDee>CcDE>ccDE>ccdee>ccDee。MN血型系统中表现型M>MN>N ;基因频率m>n,该系统中的Mur抗原阳性率特别高为22 65%(29/128) ,与上海汉族阳性率为0 66%(6/900)相比 ,怒族Mur抗原分布明显高于汉族Mur抗原。P血型系统中基因频率P2(0 7552)>P1(0 2448) ;GPC、GPA、KeLL、Wrb血型皆为阳性。结论 :不同民族的血型抗原存在一定的差异性 ,怒族的血型分布有自己的特点。     

Human RBCs blood group conversion from A to O using a novel α-N-acetylgalactosaminidase of high specific activity

α-N-acetylgalactosaminidase （αNAGA） can convert group A human red blood cells （RBCs） to group O. One novel αNAGA gene was cloned by PCR from Elizabethkingia meningosepticum Isolated from a domestic clinical sample. Pure recombinant αNAGA was obtained by genetic engineering and protein purification with a calculated molecule of 49.6 kD. αNAGA was selective for terminal α-N-acetylgalacto- samine residue with a high specific activity, αNAGA could completely remove A antigens of 1 U （about 100 mL） group A1 or A2 RBCs in 1 h at pH 6.8 and 25℃ with s consumption of 1.5 or 0.4 mg recombinant enzyme. Enzyme-converted group A RBCs did not agglutinate after being mixed with monoclonal snti-A or sere of groups A, B, AB and O. Other blood group antigens except ABO had no change. FCM analysis showed that A antigens and A1 antigens disappeared while H antigens increased. It indicated that αNAGA successfully converted human blood group A RBCs to universally transfusable group O RBCs without the risk of ABO-incompaUble transfusion reactions. This αNAGA was suitable for producing universal RBCs to increase clinical transfusion safety, improve the RBCs supply, and to decrease transfusion cost and support transfusion service in case of emergency.     

幽门螺旋杆菌感染与血型抗原相关性研究

目的通过观察幽门螺杆菌(Helicobacter pylori,Hp)在各血型患者中的分布情况,分析Hp感染与ABO血型、Lewis血型、分泌-非分泌表型的关系.方法收集幽门螺旋杆菌感染患者100例为感染组,100例健康的无偿献血者为对照组,分析两组患者的ABO血型系统、血型物质、Lewis血型系统的分布差异.结果 ABO血型分布比较:感染组O型血占56%(56/100),高于对照组的31%(31/100),感染组A型血占16%(16/100),低于对照组的33%(33/100).卡方检验结果显示:感染人群中O型血有较高发生率(56%),和普通人群中A型血(33%)之间具有显著性统计学意义(P0.05).ABO血型与幽门螺杆菌感染之间有相关性,O型人有较高感染倾向,而A型血则有较低感染倾向.Lewis表型分布比较:分析整个数据,感染组与对照组的表型分布基本一致,说明Lewis表型分布不受幽门螺杆菌感染的影响,感染组各表型与对照组比较差异无统计学意义.血型物质分布比较:分泌型个体分布在感染组和对照组之间比较差异无统计学意义.结论幽门螺杆菌感染与O型血有较强的关联,但与Lewis血型、分泌-非分泌表型无关.     

青海省湟源县日月藏族乡藏族ABO血型调查分析

本文对青海省湟源县日月藏族乡的300名藏族人群进行了ABO血型的随机抽样,其中男女各半,试图了解青海这一藏区的ABO血型分布情况和藏族族源.调查结果为:(1)藏族的ABO血型分布为A型占20.67%、B型占22.33%、O型占48.33%、AB型占8.67%|,特征是:O>B>A>AB,基因频率是p=0.1575、q=0.1673、r=0.6752,特征为r>q>p.(2)藏族ABO血型分布的民族指数为0.9991.此次调查青海省湟源县日月藏族乡的藏族人群具有较高的O基因频率,具有典型的南方人群结构特征,说明藏族与南方诸多民族有着族源关系.调查结果基本上与以往的文献资料相符,且符合我国省区血型频数分布规律.     

10例肿瘤导致ABO血型系统抗原减弱病例分析

探讨肿瘤因素导致 ABO 血型系统抗原减弱所引起的定型困难,解放军总医院2002年以来.在血型鉴定时发现10例肿瘤患者血标本,正向定型出现弱凝集或不凝集;反向定型正常,正反定型不一致.其自身对照为阴性,且排除假凝集所致.通过吸收放散、唾液型物质中和试验、H 抗原强度等实验检测弱抗原,并对患者进行随访,在患者病情缓解后重新进行血型鉴定.结果表明10例受检者红细胞上确有弱抗原存在,其中3例血清学实验呈现较明显亚型特征,但肿瘤经过治疗缓解后,亚型特征逐渐减弱甚至消失,定型恢复正常.说明某些肿瘤可以导致 ABO 血型系统抗原减弱,出现正反定型不一致,血清学呈现亚型特征,应综合病情、输血史、家系调查及特殊血清学检查来确定血型,并与亚型相鉴别.     

LaMO_3-AB_2O_4复合陶瓷材料及其复合机制的研究

研究了钙钛矿型 (ABO3 )陶瓷与尖晶石型 (AB2 O4 )陶瓷材料的复合机制 ,实验发现 :钙钛矿型陶瓷与尖晶石型陶瓷材料以一定的比例进行复合 ,在高温烧结过程中有离子迁移发生 ,离子迁移主要在B位间进行 .复合体电导率与离子迁移后所形成的结构状态有关 ,当复合体产生高电导结构时 ,复合体电阻率降低 ,反之 ,电阻率增高 .     

潮州语系人群HLA-A、B抗原及与某些疾病的关联

本文检测了60名互无血缘关系的潮州语系健康人的 HLA-A、B 抗原共28种,计算了潮州语系人群 HLA-A、B 位点的抗原频率、基因频率,及连锁不平衡的单倍型频率.初步发现潮汕语系人群的 HLA-A、B 抗原分布有不同于其他人群的一些特点,尤以All 抗原频率高的特点较为突出.在显著连锁不平衡的单倍型中,则以 A9,B60和 A2,B39两个单倍型频率较高.另外,还检测了食管癌、强直性脊柱炎、类风湿性关节炎和其它骨关节病人共142例的HLA-A、B 抗原,并研究了这些抗原与疾病的关系.结果表明除强直性脊柱炎与 B27抗原有强烈关联外,未发现其它疾病与 HLA-A、B 抗原有显著关系.本文讨论了上述结果的理论和实际意义.     

Killing of antigen-reactive B cells by class II-restricted, soluble antigen-specific CD8+ cytolytic T lymphocytes

Cytolytic T lymphocytes (CTLs) are generally thought to recognize cellular antigens presented by class I MHC molecules. A number of studies, however, have revealed responses of considerable magnitude involving both CD8+ and CD4+ CTLs with class II restriction, suggesting that class II-restricted CTLs recognizing exogeneous protein antigens may exist. As class II antigens are normally expressed on limited types of cells such as B cells and macrophages, such CTLs might be expected to exert a suppressive effect on antibody responses. Here we report that stimulation of mouse lymphocytes with a soluble antigen induced CD8+ and CD4+ CTLs specific for the antigen with class II restriction. The specific lysis was far more efficient when target B cells specifically recognized the antigen than when they did not, indicating that the primary targets for these CTLs are probably B cells expressing immunoglobulin receptors reactive for the same antigen molecule. These results suggest that the natural occurrence of such CTLs during immune responses may explain antigen-specific suppression on antibody responses by T cells.     

Selective killing of hepatitis B envelope antigen-specific B cells by class I-restricted, exogenous antigen-specific T lymphocytes

Specific B lymphocytes can act as very efficient antigen-presenting cells. They bind antigen with high affinity via their immunoglobulin receptors, process it through the class II major histocompatibility complex (MHC) pathway, and present its fragments to class II-restricted T lymphocytes. In general, exogenous antigens and noninfectious viral particles enter the class II pathway and are selectively associated with class II MHC molecules. The presentation of an exogenous antigen in association with class I molecules has been reported for only a few antigens, including the hepatitis B envelope antigen (HBenvAg). Here we demonstrate that antigen-specific B cells can efficiently deliver HBenvAg to the class I pathway, presenting its fragments to class I-restricted cytotoxic T lymphocytes (CTLs) which kill the specific B cells. This could represent a mechanism of suppression of neutralizing anti-hepatitis B virus (HBV) antibody response, a phenomenon that accompanies the development of the chronic HBV-carrier state.     

B cells acquire antigen from target cells after synapse formation

Soluble antigen binds to the B-cell antigen receptor and is internalized for subsequent processing and the presentation of antigen-derived peptides to T cells. Many antigens are not soluble, however, but are integral components of membrane; furthermore, soluble antigens will usually be encountered in vivo in a membrane-anchored form, tethered by Fc or complement receptors. Here we show that B-cell interaction with antigens that are immobilized on the surface of a target cell leads to the formation of a synapse and the acquisition, even, of membrane-integral antigens from the target. B-cell antigen receptor accumulates at the synapse, segregated from the CD45 co-receptor which is excluded from the synapse, and there is a corresponding polarization of cytoplasmic effectors in the B cell. B-cell antigen receptor mediates the gathering of antigen into the synapse and its subsequent acquisition, thereby potentiating antigen processing and presentation to T cells with high efficacy. Synapse formation and antigen acquisition will probably enhance the activation of B cells at low antigen concentration, allow context-dependent antigen recognition and enhance the linking of B- and T-cell epitopes.     

T cells can present antigens such as HIV gp120 targeted to their own surface molecules

To trigger class II-restricted T cells, antigen presenting cells have to capture antigens, process them and display their fragments in association with class II molecules. In most species, activated T cells express class II molecules; however, no evidence has been found that these cells can present soluble antigens. This failure may be due to the inefficient capture, processing or display of antigens in a stimulatory form by T-cells. The capture of a soluble antigen, which is achieved by nonspecific mechanisms in macrophages and dendritic cells, can be up to 10(3) times more efficient in the presence of surface receptors, such as surface immunoglobulin on B cells that specifically bind antigen with high affinity. We asked whether T cells would be able to present soluble antigens that bind to their own surface molecules. Here we show that such antigens can be effectively processed and presented by both CD4+- and CD8+-bearing human T cells. This indicates that T cells are fully capable of processing and displaying antigens and are mainly limited in antigen presentation by their inefficiency at antigen capture.     

新生儿病理性黄疸与ABO基因DNA多态性相关性的研究

应用等位基因特异性PCR检测71例新生儿黄疸患儿DNA的ABO血型基因型,并通过统计学分析,与255例海南汉族正常人群DNA的ABO血型基因型作对比分析,以探讨新生儿黄疸与ABO血型基因DNA多态性的相关性.结果显示:在海南籍汉族新生儿病理性黄疸患儿ABO等位基因中以A等位基因多见、O等位基因少见,在海南籍汉族新生儿病理性黄疸患儿ABO血型基因型中以AO1基因型和BO1基因型多见、BB基因型和O1O1基因型少见,与海南籍汉族正常人群对比存在显著性差异(P＜0.05).结果表明:新生儿病理性黄疸的发生可能与ABO血型基因型有关.     

湘西桑植白族ABO血型的调查报告

本文报道湘西桑植白族718人ABO血型的调查资料.结果表明:其表现型频率的次序为A>O>B>AB,基因频率的次序是O>A>AB;人群中ABO血型各型的表型频率分布分别是A 35.24%、B 25.63%、O 30.91%、AB 8.22%;基因频率为P_(0.2492) q_(0.1875)r_(0.5634);Hardy-Weiberg测验x~2=1.6.     

临夏回族ABO血型、发旋和上眼睑褶皱遗传特征的研究

对临夏500名回民的 ABO 血型、发旋和上眼睑褶皱进行了调查研究,A 型血占30.53%,B型血占31.56%、O 型血占30.33%、AB 型血占7.58%;发旋,其中单旋占93.8%、双旋占6.2%;而上眼睑褶皱,单眼睑褶皱占35.684%、双眼睑褶皱64.316%。以血型的表现型计算了其基因频率和遗传距离,认为回族与汉族的遗传距离最近。同时对血型、发旋和上眼睑褶皱之间的关系做了分析。     

A new H-2-linked class I gene whose expression depends on a maternally inherited factor

The maternally transmitted antigen (Mta) is expressed on the cells of most strains of mice. It is a medial histocompatibility antigen, that is, it is recognized by unrestricted cytotoxic T lymphocytes as are major H antigens, but unlike these it is a weak transplantation antigen and does not itself restrict the T-cell recognition of minor H antigens. All other medial H antigens are encoded by genes closely linked to the major histocompatibility complex, H-2 in the mouse. By contrast, Mta appeared to follow extrachromosomal, maternal inheritance. Several substrains of NZB, NZO and non-inbred European NMRI mice are Mta-negative. Females of these strains bear only Mta- offspring, while females of the inbred Mta+ strains bear only Mta+ offspring. Repeated backcrossing from Mta+ females to NZB or NMRI males has shown that, given the right cytoplasmic genes, the chromosomal genes of these Mta- strains permit expression of Mta2. As the Mta type of a mouse cannot be influenced by embryo transfer or foster nursing, we concluded that it was determined by a cytoplasmic factor (Mtf), transmitted through the egg. We now show that a gene, Hmt, closely linked to the H-2 complex, is also required for expression of Mta.     

Peripheral deletion of self-reactive B cells

B LYMPHOCYTES are key participants in the immune response because of their specificity, their ability to take up and present antigens to T cells, and their capacity to differentiate into antibody-secreting cells. To limit reactivity to self antigens, autospecific B cells can be functionally inactivated or deleted. Developing B cells that react with membrane antigens expressed in the bone marrow are deleted from the peripheral lymphocyte pool. It is important to ascertain the fate of B cells that recognize membrane autoantigens expressed exclusively on peripheral tissues because B cells in the peripheral lymphoid organs are phenotypically and functionally distinct from bone-marrow B cells. Here we show that in immunoglobulin-transgenic mice, B cells specific for major histocompatibility complex class I antigen can be deleted if they encounter membrane-bound antigen at a post-bone-marrow stage of development. This deletion may be necessary to prevent organ-specific autoimmunity.     

Co-adjuvant effects of retinoic acid and IL-15 induce inflammatory immunity to dietary antigens

Under physiological conditions the gut-associated lymphoid tissues not only prevent the induction of a local inflammatory immune response, but also induce systemic tolerance to fed antigens. A notable exception is coeliac disease, where genetically susceptible individuals expressing human leukocyte antigen (HLA) HLA-DQ2 or HLA-DQ8 molecules develop inflammatory T-cell and antibody responses against dietary gluten, a protein present in wheat. The mechanisms underlying this dysregulated mucosal immune response to a soluble antigen have not been identified. Retinoic acid, a metabolite of vitamin A, has been shown to have a critical role in the induction of intestinal regulatory responses. Here we find in mice that in conjunction with IL-15, a cytokine greatly upregulated in the gut of coeliac disease patients, retinoic acid rapidly activates dendritic cells to induce JNK (also known as MAPK8) phosphorylation and release the proinflammatory cytokines IL-12p70 and IL-23. As a result, in a stressed intestinal environment, retinoic acid acted as an adjuvant that promoted rather than prevented inflammatory cellular and humoral responses to fed antigen. Altogether, these findings reveal an unexpected role for retinoic acid and IL-15 in the abrogation of tolerance to dietary antigens.     

Can B cells turn on virgin T cells?

The first event in the initiation of an immune response is the capture and presentation of antigen to T cells. Such presentation involves two distinct steps: (1) display of the antigen, which requires uptake, processing and re-expression of the antigen in association with MHC molecules on the presenting cell surface; and (2) triggering, in which the presenting cell provides signals leading to the activation of the responding T cell. Two sorts of cells can capture antigens, the 'professional' antigen-presenting cells (APCs) such as dendritic cells and macrophages, and the B cells. Both types of cells can display antigens and the APCs are known to be able to trigger resting T cells. But despite in vitro evidence that certain B-cell types can reactivate previously-activated T cells, it is not yet clear whether a B cell can initiate an immune response by providing the signals necessary to activate a resting T cell. We reasoned that resting B cells should not have this capacity because of the problems this would present with tolerance to self idiotypes. By exploiting the unique properties of the avian haematopoietic system, we have examined the presenting capacity of B cells in vivo and found that resting B cells are indeed unable to activate resting T cells.     

Responses to the H-2Kba mutant involve recognition of syngeneic Ia molecules

Conventional antigens appear to be recognized by T lymphocytes only when associated with major histocompatibility complex (MHC) antigens. Using antigen-specific proliferation as a model for helper T lymphocytes, it has been demonstrated that Ly1+T cells recognize antigen presented in association with syngeneic Ia molecules. In contrast to responses to conventional antigens, however, a large number of studies have suggested that the stimulation of alloreactive Ly1+T cells, and helper T cells specific for allogeneic cytotoxic T lymphocyte (CTL) responses, involve the direct recognition of Ia alloantigens. For the generation of optimal allogeneic CTL activity it has been proposed that Ly1+T cells recognize allo-Ia antigens directly and provide help to pre-CTLs that respond to allo-H-2K and/or D determinants. Thus, the B6.C.H-2bm1 mutant (bm1, formerly referred to as Hz1), which is believed to consist of a substitution of two amino acids in the H-2Kb antigen, has presented a paradox, for it can stimulate strong mixed lymphocyte culture (MLC), graft versus host and CTL responses by T cells of H-2b haplotype mice in the apparent absence of any alloantigenic differences in the I region. We now present evidence that the stimulation of proliferative and helper T cells by the mutant B6.C.H-2bm1 results from the H-2Kba antigen being recognized in the context of syngeneic Ia determinants. Thus responses to both conventional antigens and allogeneic MHC gene products may proceed via the recognition of antigen in the context of self Ia molecules.     

Molecular components of the B-cell antigen receptor complex of the IgM class

The antigen receptors on mature B lymphocytes are membrane-bound immunoglobulins of the IgM and IgD classes whose cross-linking by polyvalent antigens results in B-cell proliferation and differentiation. How these membrane-bound immunoglobulin chains, which lack a cytoplasmic tail, generate a cell activation signal is not at present known. We now show that the IgM molecule is non-covalently associated in the membrane of B cells with two proteins of relative molecular mass 34,000 (Mr 34 K; IgM-alpha) and 39 K (Ig-beta) which form a disulphide-linked heterodimer. Surface expression of IgM seems to require the formation of an appropriate complex between IgM and the heterodimer. A transfection experiment indicates that IgM-alpha is the product of mb-1, a B-cell specific gene encoding a transmembrane protein with sequence homology to proteins of the T-cell antigen receptor-CD3 complex.