Tissue antigensPub Date : 2007-08-01DOI: 10.1055/S-2007-988408
J. Seiderer, J. Dambacher, B. Kühnlein, S. Pfennig, A. Konrad, H. Török, D. Haller, B. Göke, T. Ochsenkühn, P. Lohse, S. Brand
{"title":"The role of the selenoprotein S (SELS) gene -105G>A promoter polymorphism in inflammatory bowel disease and regulation of SELS gene expression in intestinal inflammation.","authors":"J. Seiderer, J. Dambacher, B. Kühnlein, S. Pfennig, A. Konrad, H. Török, D. Haller, B. Göke, T. Ochsenkühn, P. Lohse, S. Brand","doi":"10.1055/S-2007-988408","DOIUrl":"https://doi.org/10.1055/S-2007-988408","url":null,"abstract":"Recently, a -105G>A promoter polymorphism coding for selenoprotein S (SELS) has been shown to increase proinflammatory cytokine expression. We, therefore, analyzed SELS expression and potential phenotypic consequences of the -105G>A polymorphism in patients with inflammatory bowel disease (IBD). SELS mRNA was measured by quantitative polymerase chain reaction (PCR) in intestinal epithelial cells (IEC) after stimulation with proinflammatory cytokines and in human colonic biopsies of IBD patients as well as in murine models of ileitis and murine cytomegalovirus (MCMV) colitis. Genomic DNA from 563 individuals (Crohn's disease: n = 205; ulcerative colitis: n = 154; controls: n = 204) was analyzed for the presence of the SELS-105G>A polymorphism and the three nucleotide-binding oligomerization domain-containing protein 2 (NOD2)/caspase recruitment domain-containing protein 15 (CARD15) variants p.Arg702Trp, p.Gly908Arg and p.Leu1007fsX1008. SELS mRNA expression was increased in IEC after stimulation with proinflammatory cytokines, while its expression was not significantly altered in murine ileitis and MCMV colitis and in inflamed ileal and colonic lesions in IBD patients compared with normal controls. The SELS-105G>A polymorphism was observed with similar frequencies in IBD patients and controls and was not associated with a certain disease phenotype or serum tumor necrosis factor alpha (TNF-alpha) levels in these patients. Medium serum TNF-alpha was 1.27 pg/ml in IBD patients, while none of the controls had TNF-alpha concentrations above the detection threshold (P < 0.0001). SELS mRNA expression is upregulated by proinflammatory cytokines in IECs but the SELS-105G>A polymorphism is not associated with IBD susceptibility and does not contribute to a certain disease phenotype or increased TNF-alpha levels in IBD patients.","PeriodicalId":23105,"journal":{"name":"Tissue antigens","volume":"70 3 1","pages":"238-46"},"PeriodicalIF":0.0,"publicationDate":"2007-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"58037719","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}
Tissue antigensPub Date : 2007-05-01DOI: 10.1111/j.1399-0039.2007.00836.x
{"title":"Abstracts of the 21st European Immunogenetics and Histocompatibility Conference. Barcelona, Spain. May 5-8, 2007.","authors":"","doi":"10.1111/j.1399-0039.2007.00836.x","DOIUrl":"https://doi.org/10.1111/j.1399-0039.2007.00836.x","url":null,"abstract":"","PeriodicalId":23105,"journal":{"name":"Tissue antigens","volume":"69 5","pages":"373-532"},"PeriodicalIF":0.0,"publicationDate":"2007-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1111/j.1399-0039.2007.00836.x","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"26690100","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}
Tissue antigensPub Date : 2007-01-01DOI: 10.1111/j.1399-0039.2006.00722.x
F-M Robbins, R J Hartzman
{"title":"CD31/PECAM-1 genotyping and haplotype analyses show population diversity.","authors":"F-M Robbins, R J Hartzman","doi":"10.1111/j.1399-0039.2006.00722.x","DOIUrl":"https://doi.org/10.1111/j.1399-0039.2006.00722.x","url":null,"abstract":"<p><p>Using direct sequencing of complementary DNA products, the sequences of human CD31 from exon 1 through exon 16 of 179 individuals (139 unrelated) were systematically examined. Of the 14 biallelic single nucleotide polymorphic sites detected, 7 polymorphic sites involved amino acid substitution. These 14 polymorphic sites yielded 18 observed CD31 alleles and 9 predicted CD31 polypeptide sequences. Based on molecular haplotyping and family pedigree analysis, linkage disequilibrium among some single nucleotide polymorphic sites was observed. Single nucleotide polymorphism frequencies between populations were also measured using dot-blot hybridization with DNA or peptide nucleic acid probes.</p>","PeriodicalId":23105,"journal":{"name":"Tissue antigens","volume":"69 1","pages":"28-37"},"PeriodicalIF":0.0,"publicationDate":"2007-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1111/j.1399-0039.2006.00722.x","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"26480726","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}
Tissue antigensPub Date : 2007-01-01DOI: 10.1111/j.1399-0039.2006.00719.x
Y J Juhn, H Kita, L A Lee, R W Smith, S M Bagniewski, A L Weaver, V S Pankratz, R M Jacobson, G A Poland
{"title":"Childhood asthma and human leukocyte antigen type.","authors":"Y J Juhn, H Kita, L A Lee, R W Smith, S M Bagniewski, A L Weaver, V S Pankratz, R M Jacobson, G A Poland","doi":"10.1111/j.1399-0039.2006.00719.x","DOIUrl":"https://doi.org/10.1111/j.1399-0039.2006.00719.x","url":null,"abstract":"Little is known about the relationship between human leukocyte antigen (HLA) class II genes and family history of asthma or atopy in relation to the incidence of childhood asthma. The objective of the study was to determine whether specific HLA class II genes (e.g., DRB1*03) are associated with asthma and whether such association explains the influences of family history of asthma or atopy on asthma incidence. A stratified random sample of 340 children who had HLA data available from the Rochester Family Measles Study cohort (n= 876) and a convenience sample of healthy children aged 5-12 years were the participants. We conducted comprehensive medical record reviews to determine asthma status of these children. The associations between the presence of specific HLA alleles and development of asthma and the role of family history of asthma or atopy in the association were evaluated by fitting Cox models. The cumulative incidence of asthma by 12 years of age among children who carry HLA DRB1*03 was 33%, compared to 24.2% among those who did not carry this allele. Adjusting for family history of asthma or atopy, gender, low birth weight, season of birth, HLA DRB1*04, and HLA DQB1*0302, the hazards ratio for HLA DRB1*03 carriers was 1.8 (95% confidence interval: 1.1-2.9, P= 0.020). We concluded that the HLA DRB1*03 allele is associated with asthma. However, the HLA class II gene does not explain the influences of family history of asthma or atopy on development of asthma. The mechanism underlying the association between asthma and HLA genes needs to be elucidated.","PeriodicalId":23105,"journal":{"name":"Tissue antigens","volume":"69 1","pages":"38-46"},"PeriodicalIF":0.0,"publicationDate":"2007-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1111/j.1399-0039.2006.00719.x","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"26480727","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}
Tissue antigensPub Date : 2007-01-01DOI: 10.1111/j.1399-0039.2006.00725.x
Y Komohara, S Suekane, M Noguchi, K Matsuoka, A Yamada, K Itoh
{"title":"Expression of APOBEC3G in kidney cells.","authors":"Y Komohara, S Suekane, M Noguchi, K Matsuoka, A Yamada, K Itoh","doi":"10.1111/j.1399-0039.2006.00725.x","DOIUrl":"https://doi.org/10.1111/j.1399-0039.2006.00725.x","url":null,"abstract":"<p><p>The apolipoprotein B mRNA-editing enzyme, catalytic polypeptide-like 3G (APOBEC3G), a member of the APOBEC family possessing DNA mutator activity through cytosine deamination, is reported to play an important role in host defense against infections such as those of hepatitis B virus and human immunodeficiency virus. Here, we examined the expression of APOBEC3G in human kidney cells to better understand its biological role against infection. APOBEC3G was immunohistochemically detectable in kidney mesangial cells and also to some extent in kidney epithelial tubular cells. In addition, overexpression of APOBEC3G was shown in renal carcinoma tissues and cell lines. APOBEC3G expression was upregulated by inflammatory cytokines, such as interferon, interleukin-6, and tumor necrosis factor. These results may provide new insight into the role of APOBEC3G in host defense against viral infection and cancer.</p>","PeriodicalId":23105,"journal":{"name":"Tissue antigens","volume":"69 1","pages":"95-8"},"PeriodicalIF":0.0,"publicationDate":"2007-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1111/j.1399-0039.2006.00725.x","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"26480733","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}
Tissue antigensPub Date : 2007-01-01DOI: 10.1111/j.1399-0039.2006.00735.x
A Palikhe, J Sinisalo, M Seppänen, V Valtonen, M S Nieminen, M L Lokki
{"title":"Human MHC region harbors both susceptibility and protective haplotypes for coronary artery disease.","authors":"A Palikhe, J Sinisalo, M Seppänen, V Valtonen, M S Nieminen, M L Lokki","doi":"10.1111/j.1399-0039.2006.00735.x","DOIUrl":"https://doi.org/10.1111/j.1399-0039.2006.00735.x","url":null,"abstract":"<p><p>Aiming to study the role of human major histocompatibility complex (MHC) region on coronary artery disease (CAD), we enrolled two separate patient materials and controls. First, heart transplantation recipients (n = 276) were divided into three subgroups according to the severity of atherosclerosis. The human leukocyte antigen (HLA)-A-B-DR haplotype and gene frequencies were compared between groups. Second, patients with acute coronary syndrome (ACS) (n = 100) and healthy controls (n = 74) were assessed by nine genetic MHC markers (HLA-A, HLA-B, HLA-DRB1, LTA+253(a/g), LTA+496(C/T), LTA+633(c/g), LTA+724(C/A), C4A and C4B), and the frequencies were compared. In the heart transplantation recipients, HLA-DR1 was strongly associated with CAD [severe vs no evidence, odds ratio (OR) 2.37; 95% confidence interval (CI) 1.33-4.25; P = 0.003]. Similarly, in the patients with ACS, HLA-DRB1*01 was associated with CAD (patients vs controls, OR 2.36; 95% CI 1.25-4.44; P = 0.007). HLA-DRB1*01 was associated with low-density-lipoprotein cholesterol (OR 5.32; 95% CI 1.64-17.26; P = 0.005) and smoking habit (OR 3.13; 95% CI 1.09-9.03; P = 0.035) as risk factors. The strongest protective gene was HLA-B*07 alone (OR 0.46; 95% CI 0.24-0.88; P = 0.02) or together with the haplotype LTA+253a-LTA+633g-C4A3-C4B1 (OR 0.36; 95% CI 0.22-0.57; P = 0.00001). In conclusion, human MHC region harbors genes that protect from and predispose to CAD.</p>","PeriodicalId":23105,"journal":{"name":"Tissue antigens","volume":"69 1","pages":"47-55"},"PeriodicalIF":0.0,"publicationDate":"2007-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1111/j.1399-0039.2006.00735.x","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"26480728","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}
Tissue antigensPub Date : 2007-01-01DOI: 10.1111/j.1399-0039.2006.00732.x
A Balas, F García-Sánchez, J L Vicario
{"title":"Sequencing of a novel HLA-A allele, A*6836, showing a Bw4 epitope.","authors":"A Balas, F García-Sánchez, J L Vicario","doi":"10.1111/j.1399-0039.2006.00732.x","DOIUrl":"https://doi.org/10.1111/j.1399-0039.2006.00732.x","url":null,"abstract":"<p><p>A novel A*6836 allele was completely characterized by sequence-based typing (SBT) in a cord blood sample from an Ecuadorian donor. A*6836 discloses six clustered amino acid residue changes at the alpha-1 domain, codons 76-83, regarding its closer A*680102 allele. Therefore, A*6836 would be a new human leukocyte antigen (HLA)-A molecule showing a Bw4-epitope.</p>","PeriodicalId":23105,"journal":{"name":"Tissue antigens","volume":"69 1","pages":"99-100"},"PeriodicalIF":0.0,"publicationDate":"2007-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1111/j.1399-0039.2006.00732.x","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"26480033","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}
Tissue antigensPub Date : 2007-01-01DOI: 10.1111/j.1399-0039.2006.00701.x
J Sun, K Xu, C Wu, Y Wang, Y Hu, Y Zhu, Y Chen, Q Shi, G Yu, X Zhang
{"title":"PD-L1 expression analysis in gastric carcinoma tissue and blocking of tumor-associated PD-L1 signaling by two functional monoclonal antibodies.","authors":"J Sun, K Xu, C Wu, Y Wang, Y Hu, Y Zhu, Y Chen, Q Shi, G Yu, X Zhang","doi":"10.1111/j.1399-0039.2006.00701.x","DOIUrl":"https://doi.org/10.1111/j.1399-0039.2006.00701.x","url":null,"abstract":"<p><p>Programmed death-1 ligand-1 (PD-L1), a member of the B7 family of costimulatory molecules, plays an important role in the regulations of the cellular and humoral immune responses. In this study, two mouse anti-human PD-L1 monoclonal antibodies named 10E10 and 2H11 were successfully generated and further characterized. Monoclonal antibody 10E10 bound to distinct PD-L1 epitope comparing an available anti-PD-L1 monoclonal antibody on a series of malignant cell lines, activated T lymphocytes, B lymphocytes and dendritic cells. Then, by using immunohistochemistry staining with monoclonal antibody 2H11, the expression of PD-L1 was found in human gastric carcinoma specimens but not in normal or gastric adenoma tissues. Additional data show that PD-L1 can be regarded as a decisive factor in evaluating gastric carcinoma prognosis and anti-human PD-L1 monoclonal antibody 10E10 could inhibit T-cell apoptosis induced by tumor-associated PD-L1. Taken together, these results showed that the two functional mouse anti-human PD-L1 monoclonal antibodies we generated might be of great value for further exploration of the costimulatory molecule regulating network and immunointervention for tumor immunotherapy.</p>","PeriodicalId":23105,"journal":{"name":"Tissue antigens","volume":"69 1","pages":"19-27"},"PeriodicalIF":0.0,"publicationDate":"2007-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1111/j.1399-0039.2006.00701.x","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"26480182","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}
Tissue antigensPub Date : 2007-01-01DOI: 10.1111/j.1399-0039.2006.00728.x
B Tu, S J Mack, A Lazaro, A Lancaster, G Thomson, K Cao, M Chen, G Ling, R Hartzman, J Ng, C K Hurley
{"title":"HLA-A, -B, -C, -DRB1 allele and haplotype frequencies in an African American population.","authors":"B Tu, S J Mack, A Lazaro, A Lancaster, G Thomson, K Cao, M Chen, G Ling, R Hartzman, J Ng, C K Hurley","doi":"10.1111/j.1399-0039.2006.00728.x","DOIUrl":"https://doi.org/10.1111/j.1399-0039.2006.00728.x","url":null,"abstract":"<p><p>Sequence-based typing was used to identify human leukocyte antigen (HLA)-A, -B, -C, and -DRB1 alleles from 564 consecutively recruited African American volunteers for an unrelated hematopoietic stem cell registry. The number of known alleles identified at each locus was 42 for HLA-A, HLA-B 67, HLA-C 33, and HLA-DRB1 44. Six novel alleles (A*260104, A*7411, Cw*0813, Cw*1608, Cw*1704, and DRB1*130502) not observed in the initial sequence-specific oligonucleotide probe testing were characterized. The action of balancing selection, shaping more 'even' than expected allele frequency distributions, was inferred for all four loci and significantly so for the HLA-A and DRB1 loci. Two-, three-, and four-locus haplotypes were estimated using the expectation maximization algorithm. Comparisons with other populations from Africa and Europe suggest that the degree of European admixture in the African American population described here is lower than that in other African American populations previously reported, although HLA-A:B haplotype frequencies similar to those in previous studies of African American individuals were also noted.</p>","PeriodicalId":23105,"journal":{"name":"Tissue antigens","volume":"69 1","pages":"73-85"},"PeriodicalIF":0.0,"publicationDate":"2007-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1111/j.1399-0039.2006.00728.x","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"26480731","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}
Tissue antigensPub Date : 2007-01-01DOI: 10.1111/j.1399-0039.2006.00729.x
T L Etto, L A Stewart, J Muirhead, M Bailey, A P Schwarer
{"title":"Kappa immunoglobulin light chain polymorphisms and survival after allogeneic transplantation for B-cell malignancies: a potential graft-vs-leukaemia target.","authors":"T L Etto, L A Stewart, J Muirhead, M Bailey, A P Schwarer","doi":"10.1111/j.1399-0039.2006.00729.x","DOIUrl":"https://doi.org/10.1111/j.1399-0039.2006.00729.x","url":null,"abstract":"<p><p>In the human leucocyte antigen (HLA)-matched haematopoietic stem cell transplantation (HSCT) setting, minor histocompatibility antigen (mHA) disparities between recipient and donor can lead to graft-vs-host disease (GVHD) or graft rejection. Graft-vs-leukaemia (GVL) effect is a beneficial T-cell-mediated immune response that can also occur following HLA-matched HSCT. mHAs with tissue expression restricted to cells of the haematopoietic system are particularly relevant as immunotherapeutic targets for destroying malignant cells without inducing GVHD. Therefore, it is important to identify further haematopoietic-restricted polymorphic mHAs, which may have the potential to be used clinically for adoptive immunotherapy. Polymorphic mismatching of minor antigens, such as the B-cell-specific protein, the kappa immunoglobulin light chain (kappa) may play a role in the incidence of GVL and therefore the survival of transplant recipients following transplantation for B-cell malignancies. Polymorphisms in the constant region of the immunoglobulin kappa polypeptide chain have been defined involving single amino acid changes at positions 153 and 191. In this study, 51 HLA-matched B-cell malignancy transplant pairs were kappa typed by polymerase chain reaction and restriction enzyme digestion to investigate the association between kappa allotype disparity and outcome after transplantation. Kappa allotype disparity between transplant pairs may be associated with an increased survival compared with pairs not mismatched for kappa, as kappa mismatched recipients had a higher percentage of complete remissions and a decreased level of relapse in comparison with the nonmismatched recipients. HLA peptide prediction software was used to determine which HLA types were the best binders for kappa peptides. It was observed that patients with tissue types predicted to bind the kappa Km(1,2) peptides had better survival outcomes and no relapse compared with those with tissue types not predicted to bind the kappa Km(1,2) peptides. This study may contribute to the assessment of the clinical role of kappa with regard to the outcome of allogeneic transplantation for B-cell malignancies.</p>","PeriodicalId":23105,"journal":{"name":"Tissue antigens","volume":"69 1","pages":"56-61"},"PeriodicalIF":0.0,"publicationDate":"2007-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1111/j.1399-0039.2006.00729.x","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"26480729","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}