Academic literature on the topic 'HLA-B Antigens'
Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles
Consult the lists of relevant articles, books, theses, conference reports, and other scholarly sources on the topic 'HLA-B Antigens.'
Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.
You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.
Journal articles on the topic "HLA-B Antigens"
1
Sultana, Sharmin, Shahina Tabassum, and Afzalun Nessa. "Human Leukocyte Antigen: Class I Allele Frequencies and Haplotype Distributionin a Tertiary Care Hospital in Bangladesh." Bangladesh Medical Research Council Bulletin 44, no. 1 (June 6, 2018): 1–8. http://dx.doi.org/10.3329/bmrcb.v44i1.36798.
Full textAbstract:
Human leukocyte antigen (HLA) are cell surface glycoproteins encoded by Major Histocompatibility Complex (MHC) geneof human genome. HLA antigen frequency and haplotype distribution are useful for determining disease associations, origin, migration and genetic relationships between populations and predicting the outcome of transplantation. Thus, the present study was carried outto identify HLA class I (HLA-A and HLA-B) antigen and haplotype distribution among a selected Bangladeshi population. This retrospective study was conducted among 1070 individuals who were referred by cliniciansfor HLA typing at the Tissue Typing Laboratory of the Department of Virology, Bangabandhu Sheikh Mujib Medical University (BSMMU) during the period 2009 to 2011. For HLA typing, Blood was collected in heparin containing tube and the laboratory tests were performed by the microlymphocytotoxicity technique according to manufacturer’s instructions.Out of 19 HLA-A and 37HLA-B antigens tested, a total of 19/19 and 36/37 antigens were detectedrespectively in this study. The most frequent antigens of HLA-A and HLA-B detected were A11 (25.4%), A24 (16.6%), B75 (18.1%) and B35 (11.3%). The least antigen frequency detected for HLA-A locus were A69 (0.09%), A26 (0.28%), A34 (0.28%), while for HLA-B locus were B81 (0.09%) and B56 (0.09%). Among the HLA-A and HLA-B antigens, some alleles were found to be homozygote such as A11 (4.0%), A2 (2.7%), A24 (2.1%) andB75 (2.4%), B35 (1.8%), and B44 (1.4%) respectively. The most frequent haplotype in the study populationwereA11: B75 (4.9%). The most frequent antigens of HLA-A and HLA-B detected were A11 (25.4%), B75 (18.1%) respectively. The distribution of HLA haplotypes among the study population indicates that it has the influence of Oriental and Asian populations. Thus, this study will be helpful to provide valuable information for population genetics and HLA disease association analysis.Bangladesh Med Res Counc Bull 2018; 44(1):01-08
2
Bhowmik, Devolina, Md Ruhul Amin Miah, Shirin Tarafder, Ahmed Abu Saleh, and Manash Chandra Sarker. "Distribution of HLA-B Locus Antigens in Patients with Psoriatic Arthritis in Bangladesh." Bangladesh Journal of Medical Microbiology 12, no. 2 (August 16, 2018): 14–20. http://dx.doi.org/10.3329/bjmm.v12i2.51691.
Full textAbstract:
This study was designed to investigate the distribution of HLA-B locus antigens in patients with psoriatic arthritis (PsA) in Bangladesh and identify HLA markers related to disease manifestation in PsA. HLA-B typing was carried out by polymerase chain reaction (PCR) with sequence specific primers in a group of 50 consecutive PsA patients. The reports of HLA-B locus antigens typing were collected from 50 ages and sex matched unrelated healthy donors as controls. A total of 17 HLA-B locus antigens were determined in both patients and controls. The most common antigen was B*15 (34%) followed by B*07 (26%), B*27 (24%), B*38 (20%). Human leukocyte antigens B*07, B*27 and B*38 alleles were found to be significantly prevalent in PsA patients compared with healthy controls. We found a statistically significant association between spondylitis pattern and the presence of HLA-B*27. PsA in Bangladeshi patients seems to be associated with the presence of B*07, B*27 and B*38 alleles.
Bangladesh J Med Microbiol 2018; 12 (2): 14-20
3
Kao, KJ, DJ Cook, and JC Scornik. "Quantitative analysis of platelet surface HLA by W6/32 anti-HLA monoclonal antibody." Blood 68, no. 3 (September 1, 1986): 627–32. http://dx.doi.org/10.1182/blood.v68.3.627.627.
Full textAbstract:
Abstract Class I molecules of human major histocompatibility complex (HLA) are the most important antigenic system in determining the survival of transfused platelets in alloimmunized patients. Platelets with reduced expression of a specific type of HLA antigen may escape specific anti- HLA antibody-mediated destruction. By using 125I-labeled Fab fragments of W6/32 anti-HLA monoclonal antibody and competitive protein binding assays, we measured the range of total HLA concentrations on platelets. In 12 individuals examined, the mean number of HLA-A, B, and C molecules per platelet was 81,587 +/- 20,016 (mean +/- SD); its range was between 54,782 to 116,185 molecules per platelet. After treatment with chloroquine, 79.9 +/- 7.0% (mean +/- SD, n = 6) of HLA antigens were removed from platelets as determined by binding of 125I-W6/32 Fab. A similar result was obtained when HLA antigens on chloroquine-treated platelets were evaluated with immunofluorescence flow cytometry. In contrast, chloroquine treatment did not remove integral membrane protein such as P1A1 antigens on platelets. The presence of HLA antigens in the chloroquine eluate of platelets could be demonstrated to contain HLA antigens similar in mol wts to intact class I molecules by an immunoblotting technique. These data suggest that 70% to 80% of platelet HLA antigens are adsorbed and that such HLA antigens are not proteolytic products of integral membrane class I molecules. The origin of the adsorbed platelet HLA-antigens remains to be determined.
4
Kao, KJ, DJ Cook, and JC Scornik. "Quantitative analysis of platelet surface HLA by W6/32 anti-HLA monoclonal antibody." Blood 68, no. 3 (September 1, 1986): 627–32. http://dx.doi.org/10.1182/blood.v68.3.627.bloodjournal683627.
Full textAbstract:
Class I molecules of human major histocompatibility complex (HLA) are the most important antigenic system in determining the survival of transfused platelets in alloimmunized patients. Platelets with reduced expression of a specific type of HLA antigen may escape specific anti- HLA antibody-mediated destruction. By using 125I-labeled Fab fragments of W6/32 anti-HLA monoclonal antibody and competitive protein binding assays, we measured the range of total HLA concentrations on platelets. In 12 individuals examined, the mean number of HLA-A, B, and C molecules per platelet was 81,587 +/- 20,016 (mean +/- SD); its range was between 54,782 to 116,185 molecules per platelet. After treatment with chloroquine, 79.9 +/- 7.0% (mean +/- SD, n = 6) of HLA antigens were removed from platelets as determined by binding of 125I-W6/32 Fab. A similar result was obtained when HLA antigens on chloroquine-treated platelets were evaluated with immunofluorescence flow cytometry. In contrast, chloroquine treatment did not remove integral membrane protein such as P1A1 antigens on platelets. The presence of HLA antigens in the chloroquine eluate of platelets could be demonstrated to contain HLA antigens similar in mol wts to intact class I molecules by an immunoblotting technique. These data suggest that 70% to 80% of platelet HLA antigens are adsorbed and that such HLA antigens are not proteolytic products of integral membrane class I molecules. The origin of the adsorbed platelet HLA-antigens remains to be determined.
5
Gingrich, RD, CE Dahle, KF Hoskins, and MJ Senneff. "Identification and characterization of a new surface membrane antigen found predominantly on malignant B lymphocytes." Blood 75, no. 12 (June 15, 1990): 2375–87. http://dx.doi.org/10.1182/blood.v75.12.2375.2375.
Full textAbstract:
Abstract A monoclonal antibody, 1D10, was derived that identifies a new antigenic epitope on the surface of malignant B lymphocytes. Normal resting and stimulated lymphocytes do not express the antigen. The majority of individuals with acute Epstein-Barr virus infection express the antigen on their lymphocytes, and in these patients, the T lymphocyte may also be antigen positive. The antigen was found on B- lymphoid neoplasia from the early pre-B cell stage through terminally differentiated plasma cells, a characteristic not reported for other B cell-associated antigens. Studies on homozygous typing cells and cells from individuals with known HLA phenotypes indicate that the antigen does not segregate in a pattern characteristic for major histocompatibility antigens. The molecule is a heterodimeric polypeptide with the molecular weight and isoelectric points of the alpha and beta chains being 32,000 d/4 and 28,000 d/6, respectively. Evidence is presented that the 1D10 molecule is not HLA-DR, -DP, or - DQ. By extrapolation, we suggest that this novel molecule may represent HLA D-region gene expression of a gene(s) not normally expressed. Potential candidates are D-region pseudogenes. We conclude that the antigenic epitope identified by the 1D10 monoclonal antibody is unique among previously described B-lymphocyte antigens. Further studies of the factors controlling the expression of this molecule, as well as studies designed to look at the possible cellular function, may provide insights for understanding crucial events in the malignant transformation of lymphocytes.
6
Gingrich, RD, CE Dahle, KF Hoskins, and MJ Senneff. "Identification and characterization of a new surface membrane antigen found predominantly on malignant B lymphocytes." Blood 75, no. 12 (June 15, 1990): 2375–87. http://dx.doi.org/10.1182/blood.v75.12.2375.bloodjournal75122375.
Full textAbstract:
A monoclonal antibody, 1D10, was derived that identifies a new antigenic epitope on the surface of malignant B lymphocytes. Normal resting and stimulated lymphocytes do not express the antigen. The majority of individuals with acute Epstein-Barr virus infection express the antigen on their lymphocytes, and in these patients, the T lymphocyte may also be antigen positive. The antigen was found on B- lymphoid neoplasia from the early pre-B cell stage through terminally differentiated plasma cells, a characteristic not reported for other B cell-associated antigens. Studies on homozygous typing cells and cells from individuals with known HLA phenotypes indicate that the antigen does not segregate in a pattern characteristic for major histocompatibility antigens. The molecule is a heterodimeric polypeptide with the molecular weight and isoelectric points of the alpha and beta chains being 32,000 d/4 and 28,000 d/6, respectively. Evidence is presented that the 1D10 molecule is not HLA-DR, -DP, or - DQ. By extrapolation, we suggest that this novel molecule may represent HLA D-region gene expression of a gene(s) not normally expressed. Potential candidates are D-region pseudogenes. We conclude that the antigenic epitope identified by the 1D10 monoclonal antibody is unique among previously described B-lymphocyte antigens. Further studies of the factors controlling the expression of this molecule, as well as studies designed to look at the possible cellular function, may provide insights for understanding crucial events in the malignant transformation of lymphocytes.
7
Stern, Martin, Loredana Ruggeri, Marusca Capanni, Antonella Mancusi, and Andrea Velardi. "Human leukocyte antigens A23, A24, and A32 but not A25 are ligands for KIR3DL1." Blood 112, no. 3 (August 1, 2008): 708–10. http://dx.doi.org/10.1182/blood-2008-02-137521.
Full textAbstract:
Abstract Inhibitory killer cell immunoglobulin receptors (KIR) bind to major histocompatibility complex antigens. Concise knowledge of KIR ligands allows prediction of natural killer (NK)–cell alloreactivity after hematopoietic stem cell transplantation. KIR3DL1 binds to the Bw4 epitope on HLA-B antigens. Although the same epitope is also found on 4 HLA-A antigens (HLA-A23/24/25/32), these are not currently regarded as KIR3DL1 ligands. We show that expression of HLA A*2301, A*2402, or A*3201 but not HLA A*2501 protects target cells from lysis by KIR3DL1+ NK cells. KIR3DL1+ NK cells from donors expressing the Bw4 epitope on an HLA-A antigen only are fully functional and capable of lysing Bw4− target cells. HLA A25 differs at amino acid 90, close to the serologic Bw4 epitope, from A23/24/32 and from Bw4+ HLA-B antigens. These data suggest that HLA-A antigens should be taken into consideration when assessing the potential for NK alloreactivity after hematopoietic stem cell transplantation.
8
Popovska, Mirjana, Aneta Atanasovska-Stojanovska, Sashka Todoroska, Vera Radojkova-Nikolovska, Lindita Zendeli Bedhxeti, Ana Spasovska-Gjorgovska, Spiro Spasovski, and Marija Ivanovska-Stojanoska. "Oral Lichen Planus – Related Connection with HLA-System Antigens." PRILOZI 41, no. 1 (June 1, 2020): 65–77. http://dx.doi.org/10.2478/prilozi-2020-0024.
Full textAbstract:
AbstractAim:To determine whether there is an immunogenic connection and antigen difference between the HLA antigens in the erosive (EOLP) and reticular (ROLP) oral lichen planus.Materials and Method: 73 patients with ROLP and EOLP have been tested. Typing of the HLA antigens has been made for locus A and B. The typing of the HLA was conducted with the use of microlymphocyto toxic test by Terasaki. The reading of the findings has been conducted with an inverse microscope. When a reaction has 4 points it is considered to be positive.Results: The most frequently typified antigens in ROLP from locus A are HLA А2 (57.57%) and А3 (33.33)%, and for locus B 21.21%. In EOLP it is А9 (8888%). In locus B a connection has been found with HLA B8 (77.77%). The statistical analysis with the ×2 test has shown that the carriers of HLA A9 display a relative risk (RR) of 3.65 and ×2=20.72. Consequently, there is high static importance for locus A p<0,001. For locus B, In EOLP for HLA B8, RR=6. 7 ×2=37.64 and p<0,001. ROLP has shown association with HLA A3, where RR=2. 31 and ×2 =9.14 and p<0.05.Conclusions: In ROLP A3 antigen and in EOLP A9 and A8 may be considered as carriers with proneness to OLP.
9
Rajaei, Elham, Mohammad T. Jalali, Seyed M. Sadegh Pezeshki, Hadi Rezaeeyan, Mahmood Maniati, Milad Elyasi, and Zeinab D. Zayeri. "Dose HLA-B5, 7, 8, 27, and 51 Antigens Associated to Behcet's disease? A Study in Southwestern Iran." Current Rheumatology Reviews 16, no. 2 (May 11, 2020): 120–24. http://dx.doi.org/10.2174/1573397115666190918153721.
Full textAbstract:
Background: Behcet's disease is a potentially life threatening autoimmune disease with recurrent ulcers and unknown pathogenesis. Gender and human leukocyte antigen-B51 seem to have an effective role in the clinical features of the disease. Objective: The aim of this study is to evaluate the frequency of HLA-B5, 7, 8, 27 and 51 in behçet's disease in southwestern Iranian patients who visited the rheumatology clinic and to find the association between these HLA types and the disease. Methods: 63 patients with behcet's disease participated in this study and peripheral blood samples were collected from them. The expression of each HLA antigen was evaluated by standard lymphocytotoxicity technique. Results: Compared to other studied antigens, the expression of HLA-B5 and HLA-B51 was more prevalent among our patients. According to the results, 25% and 21% of patients were positive for HLA-B5 and HLA-B51, respectively. Conclusions: HLA-B5 and HLA-B51 are dominant positive HLA antigens among behcet's disease patients in the southwest of Iran; however, we cannot conclude that these antigens are valuable diagnostic or prognostic biomarkers due to our study limitations. We suggest studying the association between HLA-B antigens and inflammation severity in patients to determine the possible prognostic value of HLA-B antigens in Iranian population in the southwest and this region needs more studies in HLA subject among BD patients because of the frequency of BD to evaluate the value of HLA typing in BD prognosis.
10
Archbold, Julia K., Whitney A. Macdonald, Stephanie Gras, Lauren K. Ely, John J. Miles, Melissa J. Bell, Rebekah M. Brennan, et al. "Natural micropolymorphism in human leukocyte antigens provides a basis for genetic control of antigen recognition." Journal of Experimental Medicine 206, no. 1 (January 12, 2009): 209–19. http://dx.doi.org/10.1084/jem.20082136.
Full textAbstract:
Human leukocyte antigen (HLA) gene polymorphism plays a critical role in protective immunity, disease susceptibility, autoimmunity, and drug hypersensitivity, yet the basis of how HLA polymorphism influences T cell receptor (TCR) recognition is unclear. We examined how a natural micropolymorphism in HLA-B44, an important and large HLA allelic family, affected antigen recognition. T cell–mediated immunity to an Epstein-Barr virus determinant (EENLLDFVRF) is enhanced when HLA-B*4405 was the presenting allotype compared with HLA-B*4402 or HLA-B*4403, each of which differ by just one amino acid. The micropolymorphism in these HLA-B44 allotypes altered the mode of binding and dynamics of the bound viral epitope. The structure of the TCR–HLA-B*4405EENLLDFVRF complex revealed that peptide flexibility was a critical parameter in enabling preferential engagement with HLA-B*4405 in comparison to HLA-B*4402/03. Accordingly, major histocompatibility complex (MHC) polymorphism can alter the dynamics of the peptide-MHC landscape, resulting in fine-tuning of T cell responses between closely related allotypes.
Dissertations / Theses on the topic "HLA-B Antigens"
1
Hume, Clifford Robert. "Regulation of HLA class II expression in class II negative mutant B-cell lines /." Access full-text from WCMC, 1989. http://proquest.umi.com/pqdweb?did=745028251&sid=1&Fmt=2&clientId=8424&RQT=309&VName=PQD.
Full text
2
Gil, Julio Miranda. "Estudo da associação entre os alelos DR e DQ de antígenos de histocompatibilidade leucocitária (HLA) e pênfigo vulgar em pacientes brasileiros." Universidade de São Paulo, 2016. http://www.teses.usp.br/teses/disponiveis/5/5143/tde-10012017-105831/.
Full textAbstract:
INTRODUÇÃO: Pênfigo Vulgar é uma doença bolhosa mucocutânea autoimune caracterizada pela formação de bolhas ou ulcerações dolorosas que afetam as superfícies cutâneas e/ou mucosas. A perda do contato célulacélula entre os queratinócitos do epitélio (acantólise) resulta na manifestação clínica do Pênfigo Vulgar. Autoanticorpos IgG se ligam às desmogleínas - anti-desmogleína 3 (Dsg3) e/ou anti-desmogleína 1 (Dsg1) -e são críticos na patogênese da doença. A predisposição genética ao PV, principalmente com alelos HLA DR e DQ, foi revelada desde a década de 80 e foi comprovada por análises genéticas e sorológicas, repetidas vezes. As características singulares da população brasileira favorecem estudos genéticos exploratórios. PACIENTES E MÉTODO: O grupo em estudo incluiu 51 pacientes com diagnóstico confirmado de Pênfigo Vulgar de um hospital terciário da cidade de São Paulo, estado de São Paulo, sudeste do Brasil. Foi realizada a extração de DNA e a tipificação de HLA A, B, C, DR e DQ por meio de kits QIagen (QIAamp DNA Mini Kit®). O grupo controle foi composto a partir de um banco de dados de 297 doadores falecidos não relacionados da cidade de São Paulo, que foram tipados pelo mesmo método. Este banco faz parte do Sistema Estadual de Transplantes da Secretaria de Saúde do Governo do Estado de São Paulo e contém a idade do paciente na coleta. O nível de significância dos testes estatísticos foi ajustado pela correção de Bonferroni, dependendo da quantidade de frequências fenotípicas avaliadas para o HLA A, HLA B, HLA C, HLA DRB1 e HLA DQB1. RESULTADOS: Os alelos HLAB* 57, HLA-C*15, HLA-DRB1*04:02, HLA-DRB1*08:04, HLA-DRB1*14:01, DQA1*03:01, DQB1*03:02 e o DQB1*05:03 estiveram associados com a susceptibilidade. Ambos os alelos HLA DRB1*04:02 e HLA-DRB1*14:01 e seus respectivos haplótipos DRB1*04-DQA1*03:01-DQB1*03:02 e DRB1*14- DQA1*01:01-DQB1*05:03 conferiram risco à doença. DISCUSSÃO: Os alelos DRB1*04:02 e DQB1*05:03 estão associados com o Pênfigo Vulgar no presente estudo, bem como a diversas populações do mundo. A associação aqui estudada com o DRB1*08:04 foi confirmada por causa deste alelo específico e não do desequilíbrio de ligação a algum gene adjacente. A associação do alelo HLA-B*57 ao pênfigo vulgar é reportada pela primeira vez pelo presente estudo. CONCLUSÕES: Os alelos HLA-B*57, HLA-C*15, HLADRB1* 04:02, HLA-DRB1*08:04, HLA-DRB1*14:01, DQA1*03:01, DQB1*03:02 e DQB1*05:03 estão associados ao Pênfigo Vulgar em pacientes brasileirosBACKGROUND: Pemphigus vulgaris is a mucocutaneous blistering autoimune disease that manifests as painful blisters or ulcerations on the skin and/or mucosal surfaces. The loss of cell-cell adhesion among the epithelial keratinocytes (acantholisis) leads to pemphigus vulgaris clinical findings. IgG autoantibodies target desmoglein - anti-Desmoglein 3 (Dsg3) and/or 1 (Dsg1) - play a major role in the disease pathogenesis. Genetic predisposal to pemphigus vulgaris, especially the HLA DR and DQ alleles, was revealed since the 80s and has been proven through genetic and serologic analysis repeatedly. The unique constitution of the Brazilian population favours genetics exploratory studies. PATIENTS AND METHODS: The study group included fifty-one patients with confirmed diagnosis of Pemphigus Vulgaris from a tertiary hospital in Sao Paulo\'s city and state, southeast Brazil. DNA extraction and HLA A, B, C, DR and DQ typing using Qiagen kits (QIAamp DNA Mini Kit®). The control group was composed by a database of 297 unrelated deceased donors from the city of São Paulo that were typed through the same method. This database is a part of the Transplants State System of the Government\'s Health Secretary from the State of Sao Paulo. The statistical significance level was adjusted by using the Bonferroni correction depending on the phenotypic frequencies evaluated to HLA A, HLA B, HLA C, HLA DRB1 e HLA DQB1. RESULTS: The alleles HLA-B*57, HLA-C*15, HLADRB1* 04:02, HLA-DRB1*08:04, HLA-DRB1*14:01, DQA1*03:01, DQB1*03:02 and DQB1*05:03 were associated with susceptibility. Both alleles HLA DRB1*04:02 and HLA-DRB1*14:01 and their respective haplotypes DRB1*04-DQA1*03:01-DQB1*03:02 and DRB1*14-DQA1*01:01-DQB1*05:03 conferred risk to the disease. DISCUSSION: The DRB1*04:02 and DQB1*05:03 alleles are associated with Pemphigus Vulgaris in our study, as well in various populations. The association in our study with HLA-DRB1*08:04 was confirmed to be specific to this allele and not to linkage disequilibrium to any adjacent gene. The association between HLA-B*57 and pemphigus vulgaris is being reported for the first time at the present study. CONCLUSIONS: The alleles HLA-B*57, HLA-C*15, HLA-DRB1*04:02, HLADRB1* 08:04, HLA-DRB1*14:01, DQA1*03:01, DQB1*03:02 and DQB1*05:03 were associated with Pemphigus Vulgaris in Brazilian patients
3
Chiu, Angela Chen-Yen. "DNA Typing of HLA-B by PCR with Primer Mixes Utilizing Sequence-Specific Primers." Thesis, University of North Texas, 1997. https://digital.library.unt.edu/ark:/67531/metadc278947/.
Full textAbstract:
The aim of this study was to design a resolution typing system for the HLA-B gene. This technique involves a one-step PCR reaction utilizing genomic DNA and sequence-specific primers to determine the specificity of each allele and to produce a larger primer data base ideal for serological analysis. The application of this technique to serological analysis can improve serology detection which is currently hindered by antibody cross-reactivity and the unavailability of useful typing reagents.
4
Weber, Raimar. "Estudo da associação entre antígenos de histocompatibilidade leucocitária (HLA) e pênfigo vulgar em pacientes brasileiros." Universidade de São Paulo, 2010. http://www.teses.usp.br/teses/disponiveis/5/5143/tde-21122010-111128/.
Full textAbstract:
INTRODUÇÃO: O Pênfigo Vulgar é uma doença bolhosa crônica que acomente pele e mucosas. A perda de adesão epitelial ocorre por agressão autoimune às desmogleínas presentes nos desmossomos, mediada por anticorpos IgG. Estudos sobre a gênese da autoimunidade no pênfigo indicam associação entre alelos do sistema HLA, especialmente dos loci DR e DQ. A população brasileira apresenta características favoráveis a estudos exploratórios em genética decorrente de sua origem mista e intensa miscigenação. PACIENTES E MÉTODO: O grupo em estudo incluiu trinta e seis pacientes não consanguíneos com diagnóstico de Pênfigo Vulgar comprovado por imunopatologia provenientes do estado de São Paulo, Brasil. Foram tipados para os loci HLA-A, HLA-B e HLA-DR utilizando-se oligonucleotídeos sequência-específica (PCR-SSO). As frequências alélicas e fenotípicas encontradas foram comparadas com as de um grupo controle composto de dados de 712 indivíduos doadores voluntários cadastrados no Registro Nacional de Doadores de Medula Óssea (REDOME) provenientes de São Paulo e tipados pelo mesmo método. O valor de P crítico foi corrigido utilizando-se o método False Discovery Rate. RESULTADOS: Os alelos HLA-DRB1*04:02, DRB1*08:04 e DRB1*14 estiveram associados à doença com riscos relativos de 44,6, 18,6 e 4,8, respectivamente (p<0,001). Não houve diferença estatisticamente significante entre as frequências de nenhum alelo dos loci HLA-A ou HLA-B entre os grupos. DISCUSSÃO: O alelo DRB1*04:02, diretamente, e o alelo DRB1*14, indiretamente por desequilíbrio de ligação com DQB1*05:03, estão associados com Pênfigo Vulgar em diversas populações ao redor do mundo, porém nenhum estudo semelhante observou associação com o alelo DRB1*08:04 em tamanha magnitude. Acreditamos que as associações encontradas em nosso estudo não sejam decorrentes de viés de estratificação populacional. É necessária, no entanto, a tipagem de loci adjascentes ao HLA-DR dos indivíduos do grupo em estudo para diferenciar se o risco à doença é inerente a estes alelos ou a algum outro nas proximidades, com o qual estariam em desequilíbrio de ligação. CONCLUSÕES: Os alelos HLA-DRB1*04:02, DRB1*08:04 e DRB1*14 estiveram associados ao Pênfigo Vulgar em pacientes brasileiros.BACKGROUND: Pemphigus vulgaris is a chronic blistering disease affecting skin and mucous membranes. Autoimmune aggression to desmoglein in desmosomes, mediated by IgG antibodies, leads to loss of epithelial cell adhesion. Studies indicate association between some alleles of the HLA system and pemphigus vulgaris, mainly at the DR and DQ loci. Brazilian population characteristics are conducive to genetic exploratory studies because of its various origins and intense ethnically admixture. PATIENTS AND METHODS: The study group consisted of thirty-six unrelated patients with clinical and immunopathological diagnosis of pemphigus vulgaris from a tertiary hospital in Sao Paulo - Brazil. HLA allele typing at the A, B and DR loci was performed after DNA extraction using polymerase chain reaction and sequence-specific oligonucleotide probes (PCR-SSO). Allele and phenotypic frequencies were compared to those from a control group composed by 712 individuals volunteer donors registered in a national registry of bone marrow donors (REDOME) from Sao Paulo, typed using the same method. False Discovery Rate method was used to adjust level of critical P values. RESULTS: The HLADRB1* 04:02, DRB1*08:04 and DRB1*14 were associated with pemphigus vulgaris with relative risks of 44.6, 18.6 and 4.8, respectively (p <0.001). There was no significant difference between the frequencies of any allele of loci HLAA or HLA-B among the groups. DISCUSSION: The alleles DRB1*04:02 and DRB1*14 (indirectly through linkage disequilibrium with the DQB1*05:03) are associated with pemphigus vulgaris in several populations worldwide, however, no similar study reported such magnitude of association between pemphigus vulgaris and DRB1*08:04 allele. We consider that the association is not secondary to population stratification bias. HLA typing of nearby loci is required to differentiate if the association with pemphigus vulgaris is inherent to the HLA-DRB1*08:04 allele or to another gene which is in linkage disequilibrium. CONCLUSIONS: The HLA-DRB1*04:02, DRB1*08:04 and DRB1*14 were associated with pemphigus vulgaris in Brazilian patients
5
Takejima, Priscila Megumi. "Tipificação do HLA nos fenótipos alérgico e não alérgico da asma." Universidade de São Paulo, 2015. http://www.teses.usp.br/teses/disponiveis/5/5146/tde-05102015-111908/.
Full textAbstract:
A asma é uma doença heterogênea caracterizada por um processo inflamatório crônico das vias aéreas inferiores que está associado ao desenvolvimento da hiperresponsividade brônquica e remodelamento da via aérea. Atualmente, a asma é considerada uma síndrome, ou ao menos uma doença com diversos fenótipos. Tradicionalmente, dois fenótipos são bem definidos pela clínica e exames subsidiários: asma alérgica e asma não alérgica. Eles são diferentes quanto á idade de início, apresentação clínica, história pessoal e familiar de atopia e resposta ao tratamento. Ao contrário da asma alérgica, cuja fisiopatologia está bem caracterizada, a etiologia e mecanismos envolvidos na asma não alérgica não estão bem elucidados. Algumas possibilidades incluem alergia desencadeada por antígenos desconhecidos (fungos), infecção persistente (Chlamydia trachomatis, Mycoplasma sp) e auto-imunidade. Estudos têm descrito em diferentes populações associações entre a asma e alelos/antígenos HLA classe I e II, mas os resultados têm sido inconclusivos. O objetivo deste estudo foi identificar possíveis associações do antígeno leucocitário humano (HLA) classe I (A, B, C) e II (DR, DQ, DP) em pacientes brasileiros com asma alérgica e não alérgica. Um total de 109 pacientes com o diagnóstico de asma (56 com asma alérgica e 53 com asma não alérgica) que estavam em acompanhamento no Serviço de Imunologia Clínica e Alergia do Hospital das Clínicas da Faculdade de Medicina da Universidade de São Paulo, e 297 controles (doadores falecidos de órgãos sólidos) tiveram seu sistema HLA classe I (A, B e C) e II (DR, DQ e DP) tipificado. Os pacientes também realizaram espirometria e coletaram sangue para a quantificação da imunoglobulina E (IgE) sérica total e nível sérico de eosinófilos. Além disso, foram avaliados quanto à IgE específica para aeroalergenos através do teste cutâneo de puntura e a pesquisa da IgE sérica específica (ImmunoCAP). O grupo com asma alérgica foi constituído por pacientes que apresentavam resultado positivo para a pesquisa da IgE específica em ambos teste cutâneo de puntura e na investigação in vitro. E o grupo com asma não alérgica apresentava resultados negativos nos dois testes. A comparação do HLA classe I nos grupos estudados identificou frequência significativamente maior do HLA-B*42 e HLA-C*17 no grupo com asma alérgica, enquanto o HLA-B*48 estava estatisticamente associado com o fenótipo não alérgico. Na análise do HLA classe II, o HLA-DPA1*03 e HLA-DPB1*105 apresentou associação com os pacientes com asma alérgica. Concluindo, o estudo observou diferentes associações dos alelos HLA classe I e II com asma alérgica e não alérgica na população brasileira, a qual é caracterizada pela diversidade de origens e miscigenação. Porém, a predisposição genética para asma é poligênica e novos estudos em grandes populações são necessários para confirmar a associação do HLA como fator protetor ou causador da doençaAsthma is a heterogeneous chronic inflammatory disease of lower airways associated with the development of bronchial hyperresponsiveness and airway remodeling. Currently, asthma is regarded as a syndrome or at least a disease with several phenotypes.Traditionally, two phenotypes of asthma have been defined according to clinical and laboratory features: allergic and non-allergic asthma. Each of them has distint age of onset, clinical presentation, personal and family history of allergy and response to therapy. In contrast to allergic asthma, which pathophysiology is well characterized, the etiology and mechanisms involved in non-allergic asthma remain unclear. Some possibilities include allergy triggered by unknow antigens (fungi), persistent infection (Chlamydia trachomatis, Mycoplasma sp) and autoimmunity. Studies have reported associations between asthma and HLA class I and II alleles/antigens in different populations, but the results have been inconclusive. The objective of this study was to identify possible associations of the human leukocyte antigens (HLA) class I (A, B and C) and II (DR, DQ and DP) in Brazilian patients with allergic and non-allergic asthma. A total of 109 patients with asthma (56 with allergic asthma and 53 with non-allergic asthma), who were being followed at the Service of Clinical Immunology and Allergy of the Hospital das Clínicas of the University of São Paulo Medical School, and 297 controls (deceased solid organ donors) had their HLA class I (A,B and C) and II (DR, DQ and DP) typing. Patients performed spirometry and had their blood drawn to measure total serum immunoglobulin E (IgE) levels and eosinophil count. Furthermore, they were assessed for specific IgE to aeroallergens with skin prick test and serum tests (ImmunoCAP). The allergic asthma group was composed of patient presenting positive results for specific IgE in both skin prick test and in vitro assay. And the non-allergic asthma group had negative results in both tests. There were significantly higher frequencies of HLA-B*42 and HLA-C*17 in the allergic asthma group, whereas the HLA-B*48 was associated with the non-allergic group. Regarding HLA class II analysis, HLA-DPA1*03 and HLA DPB1*105 were associated with allergic asthma patients. In conclusion, the study identified different associations of HLA class I and II with allergic and non-allergic asthma in the Brazilian population, which is characterized by diversity of origins and miscegenation. However, the genetic predisposition of asthma is polygenic and new studies on large populations are needed to confirm the role of HLA as a protective or predisposing factor of disease
6
Lazaryan, Aleksandr. "Human leukocyte antigen supertypes in relation to human imunodeficiency virus infection among populations of African ancestry." Thesis, Birmingham, Ala. : University of Alabama at Birmingham, 2008. https://www.mhsl.uab.edu/dt/2009r/lazaryan.pdf.
Full text
7
Gupta, Manu. "Autoimmune markers in autoimmune diabetes /." Stockholm, 2003. http://diss.kib.ki.se/2004/91-7349-756-8/.
Full text
8
Camargo, Ulisses. "Sistemas Histo-sanguíneos ABO, Secretor e Lewis como fatores de risco para a espondilite anquilosante." Faculdade de Medicina de São José do Rio Preto, 2016. http://hdl.handle.net/tede/396.
Full textAbstract:
Submitted by Fabíola Silva (fabiola.silva@famerp.br) on 2018-02-07T18:29:25Z
No. of bitstreams: 1
ulissescamargo_tese.pdf: 700757 bytes, checksum: 68231dab9197a8717320c0e887f2b2f6 (MD5)Made available in DSpace on 2018-02-07T18:29:25Z (GMT). No. of bitstreams: 1 ulissescamargo_tese.pdf: 700757 bytes, checksum: 68231dab9197a8717320c0e887f2b2f6 (MD5) Previous issue date: 2016-09-22
Introduction. The spondyloarthritis encomprises a group of diseases strongly associated with HLA-B*27 gene. It has been proposed that genes not belonging to the major histocompatibility complex human influence the genesis of these diseases especially in patients HLA-B*27 negative. Objectives. The aim of this study was to test the hypothesis that the antigens of the ABO, Secretor and Lewis histo-blood systems are associated with spondyloarthritis, especially ankylosing spondylitis (AS). Material and methods. Three hundred and ninety-four patients with clinical suspicion of spondyloarthritis sent for identification of HLA-B*27 gene were analyzed. One hundred and nineteen (30.2%) had confirmed the diagnosis of spondyloarthritis according to the ASAS criteria. The remaining 275 (69.8%) were used as controls. The identification of HLA-B*27 gene was performed using the PCR-SSOP method. The identification of the antigens of the ABO, Secretor and Lewis histo-blood systems was performed using hemagglutination and PCR-RFLP methods. The exact Fisher's test, the chi-square, and the values of Odds Ratio (OR) and Confidence Interval set at 95% were calculated using the GraphPad INSTAT software, accepting the error of 5%. Results. No statistically significant differences were observed in the frequency of antigenic profiles of ABO (χ2: 1.152; p = 0.764; GL: 3), Secreto (χ2: 0.779; p = 0.377; GL: 1) and Lewis (χ2: 1.853; p = 0.396; GL: 2) histo-blood groups between patients and controls. The Lea antigen was more frequent in patients with AS compared to controls (OR: 1.833; 95% CI: 1025- 3284, p = 0.053). This antigen was strongly associated with AS in HLA-B*27 negative patients compared to controls (OR: 4.469; 95% CI: 1931-10342; p = 0.0007). This association remained only in males in the absence of HLA-B*27 gene (OR: 6.880; 95% CI: 1852-25564; p = 0.004). Conclusions. AS is associated to the Lea antigen in HLAB* 27 negative male patients.
Introdução. As espondiloartrites compreendem um grupo de doenças fortemente associadas ao gene HLA-B*27. Tem sido proposto que genes não pertencentes ao complexo principal de histocompatibilidade humano influenciam a gênese destas doenças especialmente nos pacientes HLA-B*27 negativos. Objetivos. O objetivo deste estudo foi testar a hipótese de que os antígenos dos sistemas histo-sanguíneos ABO, Secretor e Lewis estão associados à espondiloartrites, especialmente a espondilite anquilosante (EA). Material e método. Foram analisados 394 pacientes com suspeita clínica de espondiloartrites encaminhados para identificação do gene HLA-B*27. Cento e dezenove (30,2%) tiveram o diagnóstico de espondiloartrite confirmado de acordo com os critérios ASAS. Os 275 (69,8%) restantes compuseram o grupo controle. A identificação do gene HLA-B*27 foi realizada com o uso do método PCR-SSOP. A caracterização dos antígenos dos sistemas histo-sanguíneos ABO, Secretor e Lewis foi realizada com o uso dos métodos hemaglutinação e PCR-RFLP. O teste exato de Fisher, o qui-quadrado, os valores de Odds Ratio (OR) e do intervalo de confiança a 95% foram calculados com o uso do software GraphPad Instat, aceitando o erro de 5%. Resultados. Não foram observadas diferenças estatisticamente significantes nas frequências dos perfis antigênicos dos sistemas histo-sanguíneos ABO (χ2: 1.152; p=0,764; GL: 3), Secretor (χ2: 0.779; p=0,377; GL: 1) e Lewis (χ2: 1.853; p=0,396; GL: 2) de pacientes e controles. Foi observada maior frequência do antígeno Lea em pacientes com EA, comparados aos controles (OR: 1.833; IC 95%: 1.025 – 3.284; p=0,053). Este antígeno mostrou-se fortemente associado à EA em pacientes HLA-B*27 negativos comparados aos controles (OR: 4.469; IC 95%: 1.931 – 10.342; p=0,0007). Esta associação se manteve apenas no gênero masculino na ausência do gene HLA-B*27 (OR: 6.880; IC 95%: 1.852 – 25.564; p = 0,004). Conclusões. A EA está associada ao antígeno Lea nos pacientes masculinos HLA-B*27 negativos.
9
Townsley, Elizabeth. "CD8+ T Cell and NK Responses to a Novel Dengue Epitope: A Possible Role for KIR3DL1 in Dengue Pathogenesis: A Dissertation." eScholarship@UMMS, 2004. http://escholarship.umassmed.edu/gsbs_diss/709.
Full textAbstract:
Variation in the sequence of T cell epitopes between dengue virus (DENV) serotypes is believed to alter memory T cell responses during second heterologous infections contributing to pathology following DENV infection. We identified a highly conserved, novel, HLA-B57-restricted epitope on the DENV NS1 protein, NS126-34. We predicted higher frequencies of NS126-34-specific CD8+ T cells in PBMC from individuals undergoing secondary, rather than primary, DENV infection due to the expansion of memory CD8+T cells. We generated a tetramer against this epitope (B57-NS126-34TET) and used it to assess the frequencies and phenotype of antigen-specific T cells in samples from a clinical cohort of children with acute DENV infection established in Bangkok, Thailand. High tetramer-positive T cell frequencies during acute infection were seen in only 1 of 9 subjects with secondary infection. B57-NS126-34-specific, other DENV epitope-specific CD8+ T cells, as well as total CD8+ T cells, expressed an activated phenotype (CD69+ and/or CD38+) during acute infection. In contrast, expression of CD71 was largely limited to DENV-specific CD8+ T cells. In vitro stimulation of CD8+ T cell lines, generated against three different DENV epitopes, indicated that CD71 expression was differentially sensitive to stimulation by homologous and heterologous variant peptides with substantial upregulation of CD71 detected to peptides which also elicited strong functional responses. CD71 may therefore represent a useful marker of antigenspecific T cell activation.
During the course of our analysis we found substantial binding of B57-NS126-34 TET to CD8- cells. We demonstrated that the B57-NS126-34 TET bound KIR3DL1, an inhibitory receptor on natural killer (NK) cells. NK sensitive target cells presenting the NS126-34 peptide in the context of HLA-B57 were able to dampen functional responses of only KIR3DL1+ NK cells. Analysis of the activation of an NK enriched population in our Thai cohort revealed peak activation during the critical time phase in patients with severe dengue illness, dengue hemorrhagic fever, compared to people with mild illness.
Our data identified CD71 as biologically useful marker to study DENV-specific CD8+ T cell responses and highlighted the role of viral peptides in modulating NK cell activation through KIR-MHC class I interactions during DENV infection.
10
Townsley, Elizabeth. "CD8+ T Cell and NK Responses to a Novel Dengue Epitope: A Possible Role for KIR3DL1 in Dengue Pathogenesis: A Dissertation." eScholarship@UMMS, 2014. https://escholarship.umassmed.edu/gsbs_diss/709.
Full textAbstract:
Variation in the sequence of T cell epitopes between dengue virus (DENV) serotypes is believed to alter memory T cell responses during second heterologous infections contributing to pathology following DENV infection. We identified a highly conserved, novel, HLA-B57-restricted epitope on the DENV NS1 protein, NS126-34. We predicted higher frequencies of NS126-34-specific CD8+ T cells in PBMC from individuals undergoing secondary, rather than primary, DENV infection due to the expansion of memory CD8+T cells. We generated a tetramer against this epitope (B57-NS126-34TET) and used it to assess the frequencies and phenotype of antigen-specific T cells in samples from a clinical cohort of children with acute DENV infection established in Bangkok, Thailand. High tetramer-positive T cell frequencies during acute infection were seen in only 1 of 9 subjects with secondary infection. B57-NS126-34-specific, other DENV epitope-specific CD8+ T cells, as well as total CD8+ T cells, expressed an activated phenotype (CD69+ and/or CD38+) during acute infection. In contrast, expression of CD71 was largely limited to DENV-specific CD8+ T cells. In vitro stimulation of CD8+ T cell lines, generated against three different DENV epitopes, indicated that CD71 expression was differentially sensitive to stimulation by homologous and heterologous variant peptides with substantial upregulation of CD71 detected to peptides which also elicited strong functional responses. CD71 may therefore represent a useful marker of antigenspecific T cell activation.
During the course of our analysis we found substantial binding of B57-NS126-34 TET to CD8- cells. We demonstrated that the B57-NS126-34 TET bound KIR3DL1, an inhibitory receptor on natural killer (NK) cells. NK sensitive target cells presenting the NS126-34 peptide in the context of HLA-B57 were able to dampen functional responses of only KIR3DL1+ NK cells. Analysis of the activation of an NK enriched population in our Thai cohort revealed peak activation during the critical time phase in patients with severe dengue illness, dengue hemorrhagic fever, compared to people with mild illness.
Our data identified CD71 as biologically useful marker to study DENV-specific CD8+ T cell responses and highlighted the role of viral peptides in modulating NK cell activation through KIR-MHC class I interactions during DENV infection.
Book chapters on the topic "HLA-B Antigens"
1
Bidwell, Elizabeth A., Jeffrey L. Bidwell, Trevor J. Jones, Peter T. Klouda, Ben A. Bradley, David A. Savage, and Derek Middleton. "Restriction Fragment Length Polymorphism of HLA-DR7 Alleles and Association with HLA-B Antigens." In Immunobiology of HLA, 225–26. Berlin, Heidelberg: Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-662-39946-0_71.
Full text
2
Yang, Soo Young. "Assignment of HLA-A and HLA-B Antigens for the Reference Panel of B-Lymphoblastoid Cell Lines Determined by One-Dimensional Isoelectric Focusing (ID-IEF) Gel Electrophoresis." In Immunobiology of HLA, 43–44. New York, NY: Springer New York, 1989. http://dx.doi.org/10.1007/978-1-4612-3552-1_5.
Full text
3
de Vathaire, F., P. Herait, M. Lipinski, H. Sancho-Garnier, G. de Thé, and T. Tursz. "HLA -A, -B and -DR Antigens in North African Patients with Nasopharyngeal Carcinoma." In Epstein-Barr Virus and Human Disease, 71–72. Totowa, NJ: Humana Press, 1987. http://dx.doi.org/10.1007/978-1-4612-4590-2_15.
Full text
4
Calzia, R., M. G. Marazzi, A. Campelli, R. Piscopo, M. Dorati, F. Puppo, L. Borgiani, and M. Canepa. "Different Expression of HLA Class I Antigens in Liver of Children with Chronic Hepatitis B, Evaluated by Immunohistochemical Method." In The Immune Response to Viral Infections, 225–35. Boston, MA: Springer US, 1989. http://dx.doi.org/10.1007/978-1-4684-5712-4_22.
Full text
5
Kratzin, H., H. Götz, F. P. Thinnes, T. Kruse, H. U. Barnikol, P. Wernet, and N. Hilschmann. "Structure of Human Class II Antigens Expressed by a Homozygous Lymphoblastoid B Cell Line." In HLA Class II Antigens, 49–70. Berlin, Heidelberg: Springer Berlin Heidelberg, 1986. http://dx.doi.org/10.1007/978-3-642-70367-6_4.
Full text
6
Tsai, Sun-Lung, Ding-Shinn Chen, and Tong-Hsuan Chang. "Peptide Recognition and Competition, T Cell Receptor Usage, and HLA Restriction Elements of T Cell Clones Specific to a Determinant of Hepatitis B Virus Core and e Antigens in Chronic Type B Hepatitis." In Viral Hepatitis and Liver Disease, 162–67. Tokyo: Springer Japan, 1994. http://dx.doi.org/10.1007/978-4-431-68255-4_43.
Full text
7
Schmidt, Helmuth, Hans-Jörg Bühring, Gabriele Engler Blum, Ulrike Reichmann, Claudia Müller, Elisabeth Weiss, and Volker Gekeler. "Differential Regulation of HLA B Antigen Expression by Interferon." In Immunobiology of HLA, 155–56. Berlin, Heidelberg: Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-662-39946-0_41.
Full text
8
Penman, Alan D., Kimberly W. Crowder, and William M. Watkins. "Effectiveness of Histocompatibility Matching in High-Risk Corneal Transplantation." In 50 Studies Every Ophthalmologist Should Know, 1–8. Oxford University Press, 2020. http://dx.doi.org/10.1093/med/9780190050726.003.0001.
Full textAbstract:
The Collaborative Cornea Transplant Studies (CCTS) comprised two randomized, double-masked, clinical trials, the Antigen Matching Study (AMS) and the Crossmatch Study (CS), designed to determine whether matching HLA-A, -B, and/or HLA-DR antigens, donor-recipient crossmatching, or ABO compatibility reduced the risk of corneal allograft rejection and failure in high-risk patients. The studies showed that for patients needing a corneal graft with uncompromised immune systems and at high risk for corneal graft rejection: (1) neither HLA-A, -B, nor HLA-DR antigen matching substantially reduces the likelihood of corneal graft failure; (2) a positive donor-recipient crossmatch does not dramatically increase the risk of corneal graft failure; and (3) ABO blood group matching may be effective in reducing the risk of graft failure. Intensive steroid therapy after transplantation, frequent follow-up, medication and follow-up compliance, and patient education appear to play a significant role in corneal graft success.
9
Kam, M., and Jeffrey L. Bidwell. "Serological Typing of HLA-A, -B, and -C Antigens." In Handbook of HLA TYPING TECHNIQUES, 175–247. CRC Press, 2020. http://dx.doi.org/10.1201/9781003071846-7.
Full text
10
HSI, BAE-LI, CHANG-JING G. YEH, W. PAGE FAULK, and PETER J. STEVENS. "Transferrin Receptors, HLA-A,B,C, and Amnion Antigens in Breast Adenocarcinoma." In Protides of the Biological Fluids, 591–94. Elsevier, 1985. http://dx.doi.org/10.1016/b978-0-08-031739-7.50148-8.
Full textConference papers on the topic "HLA-B Antigens"
1
Pereira, J., C. Cretney, and R. H. Aster. "VARIABLE EXPRESSION OF ALLOANTIGENS IN PLATELET COHORTS OF DIFFERENT MEAN DENSITY:AN EFFECT OF AGING IN VIVO." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644158.
Full textAbstract:
Platelets differ widely in size and density, but the relationship of this heterogeneity to platelet age and function is not established. Published evidence suggests that platelet alloantigens of the HLA and PlA systems may be acquired by or releasedfrom platelets in the circulation. We therefore studied expression of HLA, PlAl, and other markers in platelet cohorts of high density (HD) and low density (LD) separated on a linear, isoosmotic arabinogalactan gradient. HD and LD cohorts contained 11-14% of total platelets and did not differ significantly in mean cell volume. Alloantibodies reactive with antigens P1A1, Baka, and HLA-A2 were used to saturate alloantigen sites. Surface markers were quantified (Human Immunol. 15:251, 1986) with radiolabeled monoclonalprobes specific for HLA A, B, C antigens (W6/32), the Fc fragment of IgG (Hb-43) and the glycoprotein IIb/IIIa complex (AP-2).As shown in the Table, HD platelets carry significantly more PlAl (located on GPIIIa) and significantly less HLA than LD platelets. However, HD and LD cohorts express the same number of GPIIb/IIIa and Baka (located on GPIIb) molecules. These findings are consistent with preferential loss of HLA molecules from HD- platelets in the circulation or acquisition by LD platelets. The variable expression of P1A1 in HD and LD cohorts is apparently due to a conformational change in GPIIIa, rather than acquisition or loss of the GPIIIa molecule, because total GPIIb/IIIa was thesame in the two platelet populations. Whether antigen differences in HD and LD platelets are determined at the time of platelet production or result from aging of platelets in the circulation is under investigation.
2
Reisner, H. M., E. A. Reisner, D. D. Kostyu, B. C. Lubahn, C. McMillan, and G. C. White. "POSSIBLE ASSOCIATION OF HLA AND Gm WITH THE ALLOIMMUNE RESPONSE TO FVIII." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644021.
Full textAbstract:
Between 5 and 15% of individuals with severe hemophilia A are at risk of developing inhibitors (alloantibodies) to FVIII. Genetic factors are important in determining risk, but the nature of these factors is poorly defined. The human immune response to a wide variety of antigens has been associated with the HLA and/or Gm loci. Hence, we have investigated polymorphisms at these two loci in hemophilia A patients with and without inhibitors.DATA SET: To date 127 hemophiliacs have been Gm or HLA typed. Forty-eight are inhibitor positive (I+) based on positive FVIII neutralization assays. This represents about 70% of all I+ hemophiliacs seen at UNC. To prevent familial bias, one member of each of 14 pairs of close relatives was randomly removed from the Data Set without regard to inhibitor status (Data Set 1). Twenty non-white individuals were also removed to constitute Data Set 2. GM TYPING: Samples were typed for Gm antigens 1, 3 and 5. Phenotype frequencies in Data Sets 1 and 2 did not deviate from expected values. I+ hemophiliacs showed an excess of Gm 1 in both Data Sets which was of possible significance (p = .13 and .21 respectively by chi square). Reanalysis of Data Set 2 to include only I- individuals without evidence of either circulating VIII:C or VIII:CAg (N=58) yields a p of .12. HLA TYPING: Analysis on 77 individuals in Data Set 2 (21 I+, 56 I-) has been done. In preliminary typing of HLA A, B, C, DR and DQ no significant differences in antigen frequency were found between the I+ and I- groups. INTERACTION BETWEEN HLA AND GM: A significant excess of Gm 1 I+ individuals was found among all HLA-A2 positive hemophiliacs (N=45, p=.034 by Fisher’s exact test. This was not significant after correction for multiple comparisons). This suggestion of an interaction between HLA-A2 and Gm 1 in determining alloreactivity to FVIII will require further prospective evaluation for confirmation.
3
Muszbek, L., and R. Adány. "CELLULAR DISTIBUTION OF FACTOR XIII IN HUMAN UTERUS AND PLACENTA." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644648.
Full textAbstract:
As spontaneous abortion is a frequent finding in females with Factor XIII (FXIIl) deficiency it has been presumed that the plasmatic or cellular form of this clotting factor is essential to normal fetus development. In this context it is of special interestthat FXIII subunit a has been demonstrated in the homoge-nate of human uterus and placenta by activity measurements and immunobiochemical methods. However, no information on its cellular distribution has beenpublished, so far. In the present study first FXIII subunit a was detected in paraformaldehyde-fixed, paraffin-embedded sections by immunoperoxidase technique. FXIII containing cells were localized in the connective tissue of uterus and in the mesenchyme of placental chorionic villi. Though in a single report FXIII containing connective tissue cells were interpreted as fibroblasts (Fear et al., J.Clin.Pathoi.,37,560, 1984) the mononuclear, multipolar, stellate morphological appearance of these cells suggested that they rather belong to the monocyte/macrophage cell line. To characterize them the immuno-fluorescent detection of FXIII subunit a was combined by the visualization of different marker antigens for tissue macrophages (RFDT, Leu M3, HLA-DR) and fibroblasts (IIG10) on frozen sections. The coexpression of FXIII subunit a with RFD7 and Leu M3 macrophage markers, butnot with fibroblast membrane antigen IIG10 clearly proves that FXIII containing cells both in the uterusand in the placenta are tissue macrophages. HLA-DR was strongly expressed in cells positive for FXIII subunit a. in the uterus, but not or only very weakly in the placental mesenchyme, which might be due to the relative absence of extrinsic antigens during fetal development. The morphological findings on the presence of FXIII subunit a in placental macrophages were further strengthened by immunobiochemical experiments. FXIII subunit a, but not b content of isolated placental macrophages was also verified by immunoblotting, while fibroblasts were shown to be exemptof this factor. The results well agree with our previous findings demonstrating FXIII subunit a in humanmonocytes and peritoneal macrophages (Muszbek et al., Thrombos. Res. ,37, 401,1985; Adány et al. , Eur.J.Cell Biol.,38,171,1985).
4
van Hinsbergh, V. W. M., T. Kooistra, W. Fiers, and J. J. Emeis. "TUMOR NECROSIS FACTOR INCREASES THE PRODUCTION OF PLASMINOGEN ACTIVATOR INHIBITOR IN HUMAN ENDOTHELIAL CELLS IN VITRO AND IN RATS IN VIVO." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1642858.
Full textAbstract:
The vascular endothelium plays an important role in fibrinolysis by producing tissue-type plasminogen activator (t-PA) and plasminogen activator inhibitor (PAI). The production of these factors by cultured endothelial cells (EC) is under separate control and influenced by various mediators, such as interleukin-1 (IL-1). Similar to IL-1, the monokine tumor necrosis factor (TNF) induces in EC various membrane bound components: tissue factor, HLA-A,B antigens and leukocyte adhesion molecules. We here report that TNF increased the production of PAI by human EC and increased PAI plasma levels in rats.In the presence of serum, TNF increased the production of PAI by cultured human EC from umbilical vein (2-fold) and from foreskin microvessels (2 to 10-fold). This was demonstrated by titration of t-PA to a fixed amount of EC conditioned medium, by reverse fibrin autography, and by immunoprecipitation with specific anti-PAI-1 IgG. No change in t-PA activity was found by fibrin autography. The stimulation of PAI activity by TNF was found at 4 U/ml and reached a maximum at 500 U/ml; it was not prevented by the addition of polymycin B. Stimulation of PAI production by TNF or IL-1 was observed after 2 h and sustained for at least 24 h. Separate addition of TNF or IL-1 gave similar maximal stimulation of PAI production by EC at 500 U/ml and 5 U/ml, respectively, while the addition of both mediators resulted in a 2-fold larger increase. This indicates an additive effect of TNF and IL-1. TNF did not change PAI production by human hepatocytes.To evaluate the effect of TNF in vivo, rats received a bolus injection of 250,000 U TNF/kg. Two h after injection, a 5-fold rise of circulating PAI levels was found (compared to control rats). Thereafter, the levels returned to basal values over a 10 h period. A decrease in circulating white blood cells was observed during the initial 3 h. The number of circulating platelets did not change.We conclude that stimulation of the vascular bed by TNF not only results in a change in surface characteristics of the endothelium, but also can result in systemic changes. The increase in PAI levels by TNF may decrease fibrinolysis.
5
Mbugua, Njeri. "P3.169 Human leukocyte antigen (HLA) B*18 and protection against mother- to-child hiv type1 transmission." In STI and HIV World Congress Abstracts, July 9–12 2017, Rio de Janeiro, Brazil. BMJ Publishing Group Ltd, 2017. http://dx.doi.org/10.1136/sextrans-2017-053264.404.
Full text
6
Komsalova, L. Y., A. Valdivia, and P. M. Salinas. "AB0871 Predictive values of inflammatory low back pain, positive hla b 27 antigen, increased c reactive protein, postive magnetic resonance and other features in axial spondiloarthritis (SPA). a prospective 2 years follow up." In Annual European Congress of Rheumatology, EULAR 2018, Amsterdam, 13–16 June 2018. BMJ Publishing Group Ltd and European League Against Rheumatism, 2018. http://dx.doi.org/10.1136/annrheumdis-2018-eular.1345.
Full text