Experimental and clinical immunogenetics最新文献

筛选
英文 中文
Genotyping Interleukin-10 High and Low Producers with Single-Tube Bidirectional Allele-Specific Amplification 用单管双向等位基因特异性扩增法分型白细胞介素-10高、低生产者
Experimental and clinical immunogenetics Pub Date : 2001-04-01 DOI: 10.1159/000049184
J. Karhukorpi, R. Karttunen
{"title":"Genotyping Interleukin-10 High and Low Producers with Single-Tube Bidirectional Allele-Specific Amplification","authors":"J. Karhukorpi, R. Karttunen","doi":"10.1159/000049184","DOIUrl":"https://doi.org/10.1159/000049184","url":null,"abstract":"A simple bidirectional allele-specific PCR method is described for determining the -1082 A and G alleles in the interleukin-10 (IL-10) promoter region. This polymorphism is associated with IL-10 production capacity, and it is thus interesting to see whether different infectious and autoimmune conditions are associated with it. With our method, the A and G alleles may be studied simultaneously in a single PCR reaction, as amplification of the different alleles is performed by using 3′-mismatched and partly overlapping allele-specific upstream and downstream primers around the -1082 site. The fast and simple method described here is especially suitable for large-scale association studies.","PeriodicalId":77124,"journal":{"name":"Experimental and clinical immunogenetics","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2001-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000049184","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"64621230","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 18
Interferon-Alpha Induces Transient Suppressors of Cytokine Signalling Expression in Human T Cells 干扰素- α诱导人T细胞细胞因子信号表达的瞬时抑制
Experimental and clinical immunogenetics Pub Date : 2001-04-01 DOI: 10.1159/000049186
C. Brender, M. Nielsen, C. Röpke, M. Nissen, A. Svejgaard, N. Billestrup, C. Geisler, N. Ødum
{"title":"Interferon-Alpha Induces Transient Suppressors of Cytokine Signalling Expression in Human T Cells","authors":"C. Brender, M. Nielsen, C. Röpke, M. Nissen, A. Svejgaard, N. Billestrup, C. Geisler, N. Ødum","doi":"10.1159/000049186","DOIUrl":"https://doi.org/10.1159/000049186","url":null,"abstract":"The suppressors of cytokine signalling (SOCS) proteins comprise a newly identified family of negative feedback regulators of cytokine signalling. SOCS expression is differentially induced upon cytokine stimulation in different cell types. Here we show that interferon-α (IFNα) is a potent inducer of SOCS expression in human T cells, as high expression of CIS, SOCS-1, SOCS-2, and SOCS-3 was detectable after IFNα stimulation. After 4 h of stimulation, CIS, SOCS-1, and SOCS-3 expression had returned to baseline levels, whereas SOCS-2 expression had not declined. In contrast, after IL-2 induction neither CIS, SOCS-1, nor SOCS-2 expression levels declined after 6 h. In conclusion, we provide the first evidence that IFNα induces SOCS expression in human T cells. Moreover, we show that IFNα and IL-2 induce distinct patterns of expression kinetics, suggesting that dynamic changes in cytokine sensitivity might be mediated via induction of SOCS expression with different kinetics in T cells.","PeriodicalId":77124,"journal":{"name":"Experimental and clinical immunogenetics","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2001-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000049186","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"64620914","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 46
Nomenclature of the Human Immunoglobulin Heavy (IGH) Genes 人重免疫球蛋白(IGH)基因命名法
Experimental and clinical immunogenetics Pub Date : 2001-04-01 DOI: 10.1159/000049189
M. Lefranc
{"title":"Nomenclature of the Human Immunoglobulin Heavy (IGH) Genes","authors":"M. Lefranc","doi":"10.1159/000049189","DOIUrl":"https://doi.org/10.1159/000049189","url":null,"abstract":"‘Nomenclature of the Human Immunoglobulin Heavy (IGH) Genes’, the 16th report of the ‘IMGT Locus in Focus’ section, provides the first complete list of all the human IGH genes. The total number of human IGH genes per haploid genome is 170–176 (206–212 genes, if the orphons and the processed gene are included), of which 77–84 genes are functional. IMGT/Human Genome Organization (HUGO) gene names and definitions of the human IGH genes on chromosome 14q32.33, processed gene on chromosome 9 and IGH orphons on chromosomes 15 and 16 are provided with the gene functionality and the number of alleles, according to the rules of the IMGT Scientific chart, with the accession numbers of the IMGT reference sequences and with the accession ID of the Genome Database GDB and NCBI LocusLink databases, in which all the IMGT human IGH genes have been entered. The tables are available at the IMGT Marie-Paule page of IMGT, the international ImMunoGeneTics database (http://imgt.cines.fr:8104) created by Marie-Paule Lefranc, Université Montpellier II, CNRS, France.","PeriodicalId":77124,"journal":{"name":"Experimental and clinical immunogenetics","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2001-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000049189","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"64621277","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 91
Lack of FasL Expression in Cultured Human Retinal Pigment Epithelial Cells FasL在培养的人视网膜色素上皮细胞中缺乏表达
Experimental and clinical immunogenetics Pub Date : 2001-01-01 DOI: 10.1159/000049085
C. G. Kæstel, H. Madsen, J. Prause, A. Jørgensen, Y. Liang, M. la Cour, G. Lui, N. Ødum, M. Nissen, C. Röpke
{"title":"Lack of FasL Expression in Cultured Human Retinal Pigment Epithelial Cells","authors":"C. G. Kæstel, H. Madsen, J. Prause, A. Jørgensen, Y. Liang, M. la Cour, G. Lui, N. Ødum, M. Nissen, C. Röpke","doi":"10.1159/000049085","DOIUrl":"https://doi.org/10.1159/000049085","url":null,"abstract":"Retinal pigment epithelial (RPE) cells have been proposed to play a part in maintaining the eye as an immune privileged organ. However, our knowledge of the implicated mechanism is still sparse. Fas ligand (FasL) expression of RPE cells is generally recognized to be essential for the immune privilege of the eye, but due to contradictory published results, it is unclear whether RPE cells express this molecule. The purpose of this study was to investigate the expression of FasL in RPE cells in vitro and in vivo. Cultured human fetal and adult RPE cells were examined by flow cytometry, Western blotting, RT-PCR and RNase Protection assay for FasL expression. Additionally, sections of ocular tissue were stained for FasL by immunohistochemistry. None of the used methods indicated FasL expression in cultured fetal or adult RPE cells of various passages. However, RPE cells in vivo, as judged from tissue sections, were positive for FasL, indicating a discrepancy between RPE cells in vitro and in vivo with regard to this molecule.","PeriodicalId":77124,"journal":{"name":"Experimental and clinical immunogenetics","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2001-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000049085","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"64617494","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 10
Can HLA Typing Predict the Outcome of Grass Pollen Immunotherapy? HLA分型能否预测草花粉免疫治疗的效果?
Experimental and clinical immunogenetics Pub Date : 2001-01-01 DOI: 10.1159/000049083
A. Fleva, M. Daniilidis, J. Sidiropoulos, K. Adam, A. Tourkantonis, J. Daniilidis, L. Hadzipetrou
{"title":"Can HLA Typing Predict the Outcome of Grass Pollen Immunotherapy?","authors":"A. Fleva, M. Daniilidis, J. Sidiropoulos, K. Adam, A. Tourkantonis, J. Daniilidis, L. Hadzipetrou","doi":"10.1159/000049083","DOIUrl":"https://doi.org/10.1159/000049083","url":null,"abstract":"Objective: The aim of this study was to investigate the relationship between HLA molecules and the positive or negative response of atopic patients to specific immunotherapy (SIT). Methods: We studied 42 atopic multisensitive patients undergoing grass pollen immunotherapy, 42 parents of patients (30 mothers and 12 fathers) and 173 control individuals. HLA class I and class II antigens were typed by a microlymphocytotoxicity test. The typing of DRB1* alleles for atopic patients and their parents was based on the reverse hybridization principle, while for the control group, DNA-RFLP and PCR-SSP methods were used. Results: The frequency of B14 and DRB1*1101-4 antigens/alleles, as well as the A2B5DR11 haplotype, showed a statistically significant difference in those patients who responded to immunotherapy. On the other hand, HLA-A28, B8 and DRB1*0301 antigens/alleles, as well as the frequency of the A1B8 and A1B8DR3 haplotypes, were found to be significantly higher in patients who responded poorly to SIT. Discussion: Our findings support the hypothesis that treatment responsiveness may show an association to HLA molecules, which could thus play a role in the immunological selection and monitoring of atopic patient candidacy for SIT.","PeriodicalId":77124,"journal":{"name":"Experimental and clinical immunogenetics","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2001-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000049083","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"64616953","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 6
Protein Phosphatase 2A Isotypes Regulate Cell Surface Expression of the T Cell Receptor 蛋白磷酸酶2A同型调节T细胞受体的细胞表面表达
Experimental and clinical immunogenetics Pub Date : 2001-01-01 DOI: 10.1159/000049084
J. P. Lauritsen, C. Menné, J. Kastrup, J. Dietrich, C. Geisler
{"title":"Protein Phosphatase 2A Isotypes Regulate Cell Surface Expression of the T Cell Receptor","authors":"J. P. Lauritsen, C. Menné, J. Kastrup, J. Dietrich, C. Geisler","doi":"10.1159/000049084","DOIUrl":"https://doi.org/10.1159/000049084","url":null,"abstract":"The mechanisms underlying T cell receptor (TCR) down-regulation have been extensively studied during the last decade. Whereas the importance of phosphorylation in this process has been established, it is less certain whether dephosphorylation plays a role in TCR down-regulation. In this study, we show that inhibition of the serine/threonine protein phosphatase PP2A family had a biphasic effect on TCR expression. Thus, low concentrations of PP2A inhibitors induced TCR down-regulation, whereas higher concentrations of PP2A inhibitors induced TCR up-regulation. The effect of PP2A inhibition was independent of phosphorylation of the CD3γ endocytosis motif. Whereas TCR down-regulation was caused by a partial inhibition of exocytosis, TCR up-regulation was caused by an inhibition of endocytosis. The effects on exocytosis and endocytosis were not restricted to the TCR, indicating a more general regulatory role for PP2A in both exocytosis and endocytosis.","PeriodicalId":77124,"journal":{"name":"Experimental and clinical immunogenetics","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2001-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000049084","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"64617367","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 6
Genomic Analysis of Idiopathic Infertile Patients with Sperm-Specific Depletion of CD46 精子特异性CD46缺失的特发性不孕症患者的基因组分析
Experimental and clinical immunogenetics Pub Date : 2001-01-01 DOI: 10.1159/000049086
M. Nomura, M. Kitamura, K. Matsumiya, A. Tsujimura, A. Okuyama, M. Matsumoto, K. Toyoshima, T. Seya
{"title":"Genomic Analysis of Idiopathic Infertile Patients with Sperm-Specific Depletion of CD46","authors":"M. Nomura, M. Kitamura, K. Matsumiya, A. Tsujimura, A. Okuyama, M. Matsumoto, K. Toyoshima, T. Seya","doi":"10.1159/000049086","DOIUrl":"https://doi.org/10.1159/000049086","url":null,"abstract":"Three infertile subjects with no expression of CD46 (membrane cofactor protein of complement) on their spermatozoa were found when screening 542 idiopathic male infertile patients. The sperm CD46 isoform was reported to be associated with the sperm-egg interaction, yet a ubiquitous expression of CD46 confers resistance to complement-mediated injury on host cells. All three patients expressed normal CD46 isoforms on their lymphocytes and granulocytes. Thus, the loss of CD46 is sperm-specific, probably due to testicular germ cell-specific regulation of CD46 production. Recently, a mechanism of the gene regulation of human CD46 was elucidated in which the silencer element of the 3′ UT and the promoter region of human CD46 gene partly participate. Here, we analyzed these regions of the CD46 gene in our 3 patients. We found no abnormality in 3′ and 5′ regions of the CD46 genome in the 3 patients. Thus, in these infertile patients sperm-specific depletion of CD46 is not governed by the so for identified regulators in the CD46 gene. Other unknown factors outside the known regulatory regions would play a role in the regulation of sperm-specific CD46 expression.","PeriodicalId":77124,"journal":{"name":"Experimental and clinical immunogenetics","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2001-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000049086","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"64617594","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 24
Immunoglobulin GM and KM allotypes in systemic lupus erythematosus. 系统性红斑狼疮的免疫球蛋白 GM 和 KM 异型。
Experimental and clinical immunogenetics Pub Date : 2001-01-01 DOI: 10.1159/000049190
J P Pandey, G S Cooper, E L Treadwell, G S Gilkeson, E W St Clair, M A Dooley
{"title":"Immunoglobulin GM and KM allotypes in systemic lupus erythematosus.","authors":"J P Pandey, G S Cooper, E L Treadwell, G S Gilkeson, E W St Clair, M A Dooley","doi":"10.1159/000049190","DOIUrl":"10.1159/000049190","url":null,"abstract":"<p><p>Genetic variation in immunoglobulin gamma (GM) and kappa (KM) chains was associated with systemic lupus erythematosus (SLE) in some studies. However, the data are conflicting, and only one study examined associations in African-Americans. We examined GM and KM allotypes, by race, in a population-based case-control study of SLE. Sera from patients (n = 222) and controls (n = 273) were typed for GM and KM allotypes by a hemagglutination inhibition method. GM phenotypes were not significantly associated with SLE in African-Americans or Caucasians. However, the frequency of KM phenotypes in Caucasian patients was significantly different from that in controls (p = 0.032). KM3,3 was associated with an increased risk, whereas KM1,3 was associated with a lower relative risk of SLE. In African-Americans, however, the pattern of associations with KM phenotypes differed from that in Caucasians, and the overall difference between patients and controls was not statistically significant.</p>","PeriodicalId":77124,"journal":{"name":"Experimental and clinical immunogenetics","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2001-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"64620894","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Anti-fibrillin-1 autoantibodies in systemic sclerosis are GM and KM allotype-restricted. 系统性硬化症中的抗纤连蛋白-1自身抗体受GM和KM异型限制。
Experimental and clinical immunogenetics Pub Date : 2001-01-01 DOI: 10.1159/000049191
J P Pandey, G P Page, R M Silver, E C LeRoy, C A Bona
{"title":"Anti-fibrillin-1 autoantibodies in systemic sclerosis are GM and KM allotype-restricted.","authors":"J P Pandey, G P Page, R M Silver, E C LeRoy, C A Bona","doi":"10.1159/000049191","DOIUrl":"10.1159/000049191","url":null,"abstract":"<p><p>GM and KM allotypes--genetic markers of immunoglobulin (Ig) gamma and kappa chains, respectively--have been shown to play an important role in genetic predisposition to some autoimmune diseases. To determine their role in susceptibility to systemic sclerosis (SSc; scleroderma) and in the generation of anti-fibrillin-1 antibodies, 148 SSc patients and 191 controls were typed for several GM and KM allotypes by a standard hemagglutination inhibition method. IgG and IgM antibodies to fibrillin-1 were measured by radioimmunoassay. GM and KM phenotypes were not significantly associated with SSc. However, these determinants significantly influenced the production of anti-fibrillin-1 antibodies in SSc patients. In Caucasians, GM1,3,17 23 5,13,21 and GM3 23 5,13 phenotypes were associated with the presence and absence of IgG autoantibodies, respectively. The production of these autoantibodies was also associated with KM allotypes, KM1,3 heterozygosity being associated with response and homozygosity for the KM3 allele with nonresponse to fibrillin-1. In African-Americans, the KM1 homozygotes were associated with the absence of anti-fibrillin-1 antibodies and the KM3 homozygotes with the presence of autoantibodies. In this ethnic group, the GM1,17 5,13 phenotype was associated with the absence of IgM autoantibodies. This represents the first description of genetic control of autoimmunity to fibrillin-1 in scleroderma.</p>","PeriodicalId":77124,"journal":{"name":"Experimental and clinical immunogenetics","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2001-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"64621415","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Molecular Analysis of Plasma α1,3-Fucosyltransferase Deficiency and Development of the Methods for Its Genotyping 血浆α1,3-聚焦转移酶缺乏的分子分析及其基因分型方法的发展
Experimental and clinical immunogenetics Pub Date : 2001-01-01 DOI: 10.1159/000049082
Susumu Tanaka, S. Yazawa, Kasumi Noguchi, T. Nishimura, K. Miyanaga, N. Kochibe, D. Poland, W. van Dijk, K. Matta
{"title":"Molecular Analysis of Plasma α1,3-Fucosyltransferase Deficiency and Development of the Methods for Its Genotyping","authors":"Susumu Tanaka, S. Yazawa, Kasumi Noguchi, T. Nishimura, K. Miyanaga, N. Kochibe, D. Poland, W. van Dijk, K. Matta","doi":"10.1159/000049082","DOIUrl":"https://doi.org/10.1159/000049082","url":null,"abstract":"Four patients with mental illness were found to be deficient in plasma α1,3-fucosyltransferase for the first time in Japan [Exp Clin Immunogenet 1999;16:125–130]. Complete sequencing of FUT6 genes in these individuals revealed the presence of two point mutations, i.e., G739 to A (Glu→247 to Lys) and C945 to A (Tyr→315 to stop). In addition to two reported alleles having G739 to A (pf1) and G739 to A and C945 to A (pf3), a new mutated allele having C945 to A (pf2) was found to be present and all the individuals who lack α1,3-fucosyltransferase activity in plasma were found to possess pf genes homozygously (pf/pf). In order to detect such lethal mutations in FUT6 genes easily, PCR-RFLP methods have also been developed and applied for the screening of FUT6 deficiency in a large number of samples which resulted in the demonstration of three additional FUT6-deficient individuals. The absence of α1,3-fucosylated molecules on α1-acid glycoprotein in plasma from all the 7 individuals was confirmed to result from the plasma α1,3-fucosyltransferase deficiency.","PeriodicalId":77124,"journal":{"name":"Experimental and clinical immunogenetics","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2001-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000049082","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"64616891","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 12
0
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
确定
请完成安全验证×
相关产品
×
本文献相关产品
联系我们:info@booksci.cn Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术官方微信