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8. World human neutrophil antigens investigation survey

Author

Bayat, Behnaz, primary, Lowack, Jonas, additional, Audrain, Marie, additional, Croisille, Laure, additional, Curtis, Brian, additional, Dangerfield, Rebecca, additional, Esmaeili, Behnaz, additional, Grabowski, Claudia, additional, Keller, Margaret, additional, Kim, Hyungsuk, additional, Kroll, Hartmut, additional, Kvanka, Marjeta Macek, additional, Kwok, Janette, additional, Moritz, Elyse, additional, Nathalang, Oytip, additional, Nelson, Derrick, additional, Nielsen, Kaspar René, additional, Pahn, Gail, additional, Poles, Anthony, additional, Porcelijn, Leendert, additional, Sachs, Ulrich J., additional, Schönbacher, Marlies, additional, Körmöczi, Günther F., additional, Kupatawintu, Pawinee, additional, Takahashi, Daisuke, additional, Uhrynowska, Malgorzata, additional, Flesch, Brigitte, additional, and Fung, Yoke‐Lin, additional

Published
2023
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18. Immunization against α β and α β in Glanzmann thrombasthenia patients carrying the French Gypsy mutation

Author

Fiore, Mathieu, BAYAT, Behnaz, PHUANGTHAM, Roongaroon, BLOUIN, Laura, Huguenin, Yoann, BEIN, Gregor, SANTOSO, Sentot, Biologie des maladies cardiovasculaires = Biology of Cardiovascular Diseases, and Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Bordeaux (UB)-Centre National de la Recherche Scientifique (CNRS)

Subjects
endocrine system, transfusion medicine, GP IIb/IIIa, integrins, inherited/acquired platelet disorders, hormones, hormone substitutes, and hormone antagonists, endothelial cells, [SDV.MHEP]Life Sciences [q-bio]/Human health and pathology
Abstract

Essentials The c.1544+1G>A mutation was identified in Gypsy Glanzmann thrombasthenia (GT) patients. Gypsy GT patients express normal α β carrying HPA-1b epitopes. To demonstrate HPA-1a alloimmunization by modified antigen capture assays. Gypsy GT patients could develop anti-HPA-1a alloantibodies against β and α β . ABSTRACT: Background Glanzmann thrombasthenia (GT) is a rare bleeding disorder caused by the absence or the dysfunction of the platelet α β integrin. A founder mutation in the ITGA2B gene was previously identified in French Gypsy patients. Interestingly, this mutation was strongly linked to the human platelet antigen-1b (HPA-1b). The HPA-1bb Gypsy patients are at risk of isoimmunization against α β , as this complex is not expressed at their platelet surface. Tentatively, they would, however, not have an increased risk of developing anti-HPA-1a alloantibodies by exposure of α β on platelets from random platelet transfusions. However, the β chain can also associate with the α subunit expressed at the platelet surface. Because Gypsy GT patients express normal α β carrying HPA-1b epitopes, these patients might develop anti-HPA-1a alloantibodies reacting with α β and/or β . Objectives/Patients/Methods To demonstrate this hypothesis, sera from HPA-1bb (n = 5) and HPA-1ab (n = 1) Gypsy GT patients were investigated by modified antigen capture assay using platelets or stable transfected cells. Furthermore, stable transfected cells expressing either α β or α β3 together with soluble monomeric chimeric β (as absorbent) were used to differentiate anti-β and anti-α β reactivity. Results Only HPA-1bb patients developed alloantibodies reacting with HPA-1a cells. Further analysis showed that HPA-1bb patients developed anti-HPA-1a alloantibodies reacting with β and/or α β . Conclusion In this study, we found that HPA-1bb patients who failed to express α β on the platelet surface can develop alloantibodies against HPA-1a reacting with β as well as α β . This is of particular importance as anti-HPA-1a alloantibodies might cause fetal neonatal alloimmune thrombocytopenia and/or platelet transfusion refractoriness.

Published
2021

24. CYP1B1 Mutation Profile of Iranian Primary Congenital Glaucoma Patients and Associated Haplotypes

Author

Chitsazian, Fereshteh, Tusi, Betsabeh Khoramian, Elahi, Elahe, Saroei, Heidar Amini, Sanati, Mohammad H., Yazdani, Shahin, Pakravan, Mohammad, Nilforooshan, Navid, Eslami, Yadollah, Mehrjerdi, Mohammad Ali Zare, Zareei, Reza, Jabbarvand, Mahmood, Abdolahi, Ali, Lasheyee, Ali R., Etemadi, Arash, Bayat, Behnaz, Sadeghi, Mehdi, Banoei, Mohammad M., Ghafarzadeh, Behnam, Rohani, Mohammad R., Rismanchian, Akram, Thorstenson, Yvonne, and Sarfarazi, Mansoor

Published
2007
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25. Naturally occurring point mutationCys460Trplocated in theI‐EGF1domain of integrin β3 alters the binding of someanti‐HPA‐1aantibodies

Author

Holzwarth, Sarah Theresa, primary, Bayat, Behnaz, additional, Zhu, Jieqing, additional, Phuangtham, Roongaroon, additional, Fischer, Lars, additional, Boeckelmann, Doris, additional, Röder, Lida, additional, Berghöfer, Heike, additional, Schmidt, Silke, additional, Bein, Gregor, additional, and Santoso, Sentot, additional

Published
2020
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30. FcγRI and FcγRIII on splenic macrophages mediate phagocytosis of anti-glycoprotein IIb/IIIa autoantibody-opsonized platelets in immune thrombocytopenia

Author

Norris, Peter A. A., primary, Segel, George B., additional, Burack, W. Richard, additional, Sachs, Ulrich J., additional, Lissenberg-Thunnissen, Suzanne N., additional, Vidarsson, Gestur, additional, Bayat, Behnaz, additional, Cserti-Gazdewich, Christine M., additional, Callum, Jeannie, additional, Lin, Yulia, additional, Branch, Donald, additional, Kapur, Rick, additional, Semple, John W., additional, and Lazarus, Alan H., additional

Published
2020
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33. Multicenter Study on Differential Human Neutrophil Antigen 2 Expression and Underlying Molecular Mechanisms

Author

Flesch, Brigitte K., primary, Reil, Angelika, additional, Nogués, Núria, additional, Canals, Carme, additional, Bugert, Peter, additional, Schulze, Torsten J., additional, Huiskes, Elly, additional, Porcelijn, Leendert, additional, Höglund, Petter, additional, Ratcliffe, Paul, additional, Schönbacher, Marlies, additional, Kerchrom, Hans, additional, Kellershohn, Josina, additional, and Bayat, Behnaz, additional

Published
2020
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40. The non-conservative CD177 SNP c.1291G>A is a genetic determinant for HNA-2 atypical/low expression and deficiency

Author

Wu, Jianming, Li, Yunfang, Schuller, Randy M., Li, Ling, Litmeyer, Anne-Sophie, Bein, Gregor, Sachs, Ulrich J, and Bayat, Behnaz

Subjects
Isoantigens, DNA, Complementary, Base Sequence, Genotype, Neutrophils, Humans, Female, Receptors, Cell Surface, Flow Cytometry, GPI-Linked Proteins, Polymorphism, Single Nucleotide, Article
Abstract

BACKGROUND: Human neutrophil antigen-2 (HNA-2) is exclusively expressed on neutrophils. HNA-2 deficient individuals (HNA-2 null) are susceptible to produce isoantibodies. The nonsense CD177 coding SNP c.787 A>T has been demonstrated as the primary genetic mechanism for HNA-2 deficiency. We hypothesized that the other genetic variants also contribute to HNA-2 expression and deficiency. STUDY DESIGN AND METHODS: The deficiency, density, and percentage of HNA-2 antigen on neutrophils from 292 healthy blood donors were determined in flow cytometry. CD177 genotypes were determined by genomic DNA sequence analyses. The full-length CD177 cDNAs were amplified and sequenced. Additionally, the whole CD177 genomic sequence in eight HNA-2 null immunized women and four HNA-2 positive donors were analyzed with next-generation sequencing (NGS). The associations of CD177 SNP genotypes with HNA-2 expression variation were statistically analyzed. RESULTS: A functional CD177 SNP c.1291G>A was identified in the current study. Atypical (trimodal) HNA-2 expression phenotype was consistently observed in donors carrying the heterozygous c.1291G/A genotype. Phenotype-genotype analyses of SNP c.787A>T and SNP c.1291G>A revealed that all homozygous 787T-1291G (TG/TG) genotype donors were HNA-2 null in healthy blood donors. On the other hand, five out of eight HNA-2 immunized females were homozygous for the 787T-1291G (TG/TG) genotype while the other three HNA-2 immunized females had the 787T-1291G/787A-1291A (TG/AA) genotype and the lowest HNA-2 expressions were observed in healthy subjects with the 787T-1291G/787A-1291A (TG/AA) and 787A-1291A/787A-1291A (AA/AA) genotype. CONCLUSION: The CD177 SNP c.1291G>A is a genetic determinant for the atypical and low HNA-2 expressions, which also contribute to HNA-2 deficiency phenotype.

Published
2019

41. Glycoprotein V is a relevant immune target in patients with immune thrombocytopenia

Author

Vollenberg, Richard, primary, Jouni, Rabie, additional, Norris, Peter A. A., additional, Burg-Roderfeld, Monika, additional, Cooper, Nina, additional, Rummel, Mathias J., additional, Bein, Gregor, additional, Marini, Irene, additional, Bayat, Behnaz, additional, Burack, Richard, additional, Lazarus, Alan H., additional, Bakchoul, Tamam, additional, and Sachs, Ulrich J., additional

Published
2019
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44. Fcγ Receptors I and III on Splenic Macrophages Mediate GPIIb/IIIa Autoantibody-Dependent Phagocytosis of Platelets in Human Immune Thrombocytopenia

Author

Norris, Peter A. A., primary, Segel, George B., additional, Sachs, Ulrich J, additional, Bayat, Behnaz, additional, Vidarsson, Gestur, additional, Kapur, Rick, additional, Cserti-Gazdewich, Christine M., additional, Callum, Jeannie, additional, Lin, Yulia, additional, Burack, Richard, additional, Semple, John W, additional, and Lazarus, Alan H, additional

Published
2018
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45. Naturally occurring point mutation Cys460Trp located in the I-EGF1 domain of integrin β3 alters the binding of some anti-HPA-1a antibodies.

Author

Holzwarth, Sarah Theresa, Bayat, Behnaz, Zhu, Jieqing, Phuangtham, Roongaroon, Fischer, Lars, Boeckelmann, Doris, Röder, Lida, Berghöfer, Heike, Schmidt, Silke, Bein, Gregor, and Santoso, Sentot

Subjects
*EPIDERMAL growth factor, *IMMUNOGLOBULINS, *INTEGRINS, *FLOW cytometry, *CELL lines, *RESEARCH, *GENETIC mutation, *RESEARCH methodology, *GENETIC disorders, *MEDICAL cooperation, *EVALUATION research, *COMPARATIVE studies, *BLOOD coagulation disorders, *RESEARCH funding, *AMINO acids, *EPITHELIAL cells, *ANTIGENS
Abstract

Background: Fetal and neonatal alloimmune thrombocytopenia (FNAIT) is caused by the destruction of platelets in the fetus or newborn by maternal platelet alloantibodies, mostly against human platelet antigen (HPA)-1a. Recent studies indicate that two anti-HPA subtypes exist: Type I reacts with epitopes residing on the plexin-semaphorin-integrin (PSI) and type II with plexin-semaphorin-integrin/integrin epidermal growth factor 1 (I-EGF1) domains of the β3 integrin. Here, we evaluated whether a Cys460Trp mutation in the I-EGF1 domain found in a patient with Glanzmann thrombasthenia can alter the binding of anti-HPA-1a.Methods: Stable HEK293 cell lines expressing wild-type and mutant αIIbβ3 and αvβ3 were generated to prove the reactivity of different antibodies against HPA-1a.Results: Flow cytometry analysis of wild-type (Cys460) and mutant (Trp460) expressed on HEK293 cells showed equal surface expression of αIIbβ3 and αvβ3. When tested with mutant αIIbβ3 cells, reduced binding was observed in Type II but not in Type I anti-HPA-1a. These results could be confirmed with platelets carrying Cys460Trp mutation. Interestingly, reduced binding of Type I antibodies was detected with mutant αvβ3 cells. Both antibody types were found in maternal sera from FNAIT cases by an antigen-capture assay with use of HEK293 transfected cells.Conclusions: These observations confirm the existence of Type I and Type II anti-HPA-1a. Furthermore, this study underlines different immunogenicity of HPA-1a antigen(s) residing on either αIIbβ3 or αvβ3. Further analysis of FNAIT cases from mothers having a fetus with and without intracranial bleedings with use of such an approach may highlight the functional relevance of different anti-HPA-1a subtypes. [ABSTRACT FROM AUTHOR]

Published
2020
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46. Gene frequencies of human platelet antigen-1 to -5 and -15 in the Iranian population.

Author

Shaiegan, Mojgan, Ghasemi, Ali, Madani, Tahereh, Samiee, Shahram, Bayat, Behnaz, Mohammadi, Saeed, and Zadsar, Maryam

Abstract

Background As the frequency of human platelet antigens varies between different ethnic groups and the data about the HPA gene frequency in Iran have been absent yet, the purpose of this study was to determine HPA-1 to HPA-5 and HPA-15 allele frequency among Iranians. Materials and methods HPA-1, HPA-2, HPA-3, HPA-4, HPA-5 and HPA-15 typing was performed by the polymerase chain reaction–sequence-specific primer techniques (PCR-SSP) for 210 subjects [Including 100 blood donors, 55 hematopoietic stem cell (HSC) recipient/donor pairs]. Results The frequencies of HPA phenotypes were determined as follows: HPA- 1a/1a: 98%, HPA-1a/1b:2%, HPA-2a/2a: 8/.5%, HPA-2a/2b: 91·5%, HPA-3a/3a: 21%, HPA-3a/3b: 67·2%, HPA-3b/3b: 22·8%, HPA-4a/4a: 100%, HPA-5a/5a: 99·5%, HPA-5a/5b: 0·5%, HPA-15a/15a: 14·2%, HPA-15a/15b: 67·2% and HPA- 15b/15b: 18·6%. Conclusion HPA-4b was absent and there was not any homozygosity for HPA- 1b/1b, HPA-2b/2b and HPA-5b/5b besides no HPA-1b/b, HPA-2b/b and HPA-5b/ b homozygosity was found. So it seems that HPA-1a, HPA-2a, HPA-4a and HPA-5a might not be involved in the alloimmunization and transfusion reactions on the Iranian population but HPA-15a and HPA3a. Furthermore, extensive studies covering diverse ethnic groups, in the field of platelet immunobiology, will help to find the local pattern more precisely. [ABSTRACT FROM AUTHOR]

Published
2020
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48. Immunization against αIIbβ3and αvβ3in Glanzmann thrombasthenia patients carrying the French Gypsy mutation

Author

Fiore, Mathieu, Bayat, Behnaz, Phuangtham, Roongaroon, Blouin, Laura, Huguenin, Yoann, Bein, Gregor, and Santoso, Sentot

Abstract

EssentialsThe c.1544+1G>A mutation was identified in Gypsy Glanzmann thrombasthenia (GT) patients.Gypsy GT patients express normal αvβ3carrying HPA‐1b epitopes.To demonstrate HPA‐1a alloimmunization by modified antigen capture assays.Gypsy GT patients could develop anti‐HPA‐1a alloantibodies against β3and αvβ3. The c.1544+1G>A mutation was identified in Gypsy Glanzmann thrombasthenia (GT) patients.Gypsy GT patients express normal αvβ3carrying HPA‐1b epitopes.To demonstrate HPA‐1a alloimmunization by modified antigen capture assays.Gypsy GT patients could develop anti‐HPA‐1a alloantibodies against β3and αvβ3. Glanzmann thrombasthenia (GT) is a rare bleeding disorder caused by the absence or the dysfunction of the platelet αIIbβ3integrin. A founder mutation in the ITGA2Bgene was previously identified in French Gypsy patients. Interestingly, this mutation was strongly linked to the human platelet antigen‐1b (HPA‐1b). The HPA‐1bb Gypsy patients are at risk of isoimmunization against αIIbβ3, as this complex is not expressed at their platelet surface. Tentatively, they would, however, not have an increased risk of developing anti‐HPA‐1a alloantibodies by exposure of αIIbβ3on platelets from random platelet transfusions. However, the β3chain can also associate with the αvsubunit expressed at the platelet surface. Because Gypsy GT patients express normal αvβ3carrying HPA‐1b epitopes, these patients might develop anti‐HPA‐1a alloantibodies reacting with αvβ3and/or β3. To demonstrate this hypothesis, sera from HPA‐1bb (n = 5) and HPA‐1ab (n = 1) Gypsy GT patients were investigated by modified antigen capture assay using platelets or stable transfected cells. Furthermore, stable transfected cells expressing either αIIbβ3or αvβ3 together with soluble monomeric chimeric β3(as absorbent) were used to differentiate anti‐β3and anti‐αvβ3reactivity. Only HPA‐1bb patients developed alloantibodies reacting with HPA‐1a cells. Further analysis showed that HPA‐1bb patients developed anti‐HPA‐1a alloantibodies reacting with β3and/or αvβ3. In this study, we found that HPA‐1bb patients who failed to express αIIbβ3on the platelet surface can develop alloantibodies against HPA‐1a reacting with β3as well as αvβ3. This is of particular importance as anti‐HPA‐1a alloantibodies might cause fetal neonatal alloimmune thrombocytopenia and/or platelet transfusion refractoriness.

Published
2021
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50. The nonconservative CD177 single-nucleotide polymorphism c.1291G>A is a genetic determinant for human neutrophil antigen-2 atypical/low expression and deficiency.

Author

Wu, Jianming, Li, Yunfang, Schuller, Randy M., Li, Ling, Litmeyer, Anne‐Sophie, Bein, Gregor, Sachs, Ulrich J, Bayat, Behnaz, and Litmeyer, Anne-Sophie

Subjects
NEUTROPHIL immunology, DNA analysis, NUCLEOTIDE sequence, FLOW cytometry, GENOTYPES
Abstract

Background: Human neutrophil antigen-2 (HNA-2) is exclusively expressed on neutrophils. HNA-2-deficient individuals (HNA-2 null) are susceptible to produce isoantibodies. The nonsense CD177 coding single-nucleotide polymorphism (SNP) c.787A>T has been demonstrated as the primary genetic mechanism for HNA-2 deficiency. We hypothesized that the other genetic variants also contribute to HNA-2 expression variation and deficiency.Study Design and Methods: The deficiency, density, and percentage of HNA-2 antigen on neutrophils from 292 healthy blood donors were determined in flow cytometry. CD177 genotypes were determined by genomic DNA sequence analyses. The full-length CD177 cDNAs were amplified and sequenced. Additionally, the whole CD177 genomic sequence in eight HNA-2-null immunized women and four HNA-2-positive donors were analyzed with next-generation sequencing. The associations of CD177 SNP genotypes with HNA-2 expression variation were statistically analyzed.Results: A functional CD177 SNP c.1291G>A was identified in the current study. Atypical (trimodal) HNA-2 expression phenotype was consistently observed in donors carrying the heterozygous c.1291G/A genotype. Phenotype-genotype analyses of SNP c.787A>T and SNP c.1291G>A revealed that all homozygous 787T-1291G (TG/TG) genotype donors were HNA-2 null in healthy blood donors. On the other hand, five of eight HNA-2-immunized females were homozygous for the 787T-1291G (TG/TG) genotype while the other three HNA-2-immunized females had the 787T-1291G/787A-1291A (TG/AA) genotype and the lowest HNA-2 expression was observed in healthy subjects with the 787T-1291G/787A-1291A (TG/AA) and 787A-1291A/787A-1291A (AA/AA) genotype.Conclusion: The CD177 SNP c.1291G>A is a genetic determinant for the atypical and low HNA-2 expression, which also contributes to HNA-2 deficiency phenotype. [ABSTRACT FROM AUTHOR]

Published
2019
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