Relevant bibliographies by topics / Blood Group Incompatibility – immunology

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Academic literature on the topic 'Blood Group Incompatibility – immunology'

Author: Grafiati
Published: 4 June 2021
Last updated: 11 February 2022

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Journal articles on the topic "Blood Group Incompatibility – immunology"

1

OGBIMI, A., G. OYEYINKA, and A. OMU. "ABO blood group incompatibility and infertility in Nigerian couples." Immunology Letters 14, no. 4 (April 1987): 299–301. http://dx.doi.org/10.1016/0165-2478(87)90008-3.

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Siqi, Cheng, Baolin Tang, Xiaoyu Zhu, Huilan Liu, Kaidi Song, Xiang Wan, Wen Yao, Jian Wang, and Zimin Sun. "Impact of ABO Blood Group Incompatibility on Outcomes after Single-Unit Umbilical Cord Blood Transplantation for Malignant Hematological Disease." Blood 134, Supplement_1 (November 13, 2019): 2055. http://dx.doi.org/10.1182/blood-2019-130699.

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Objective In contrast to solid organ transplantation, ABO blood group incompatibility was acceptable in allogeneic hematopoietic stem cell transplantation (allo-HSCT). However, reports of the effect of donor-recipient ABO incompatibility on long-time survival, graft-versus-host disease (GVHD), and relapse after allo-HSCT were controversial. Relatively few reports existed on the effects of ABO incompatibility after umbilical cord blood transplantation (UCBT). The aim of this study was to investigate the role of major ABO incompatibility on RBC transfusion burden, hematologic recovery, GVHD, transplant-related mortality (TRM), relapse, and overall survival (OS) in UCBT for malignant disease. Methods This retrospective study included 587 malignant hematonosis patients who received myeloablative single-unit unrelated donor UCBT at our center between May 2008 and June 2018. Median follow-up time of the patients alive was 40.7 months (range: 12.0-134.6 months). A total of 230 (39.2%) patients received an ABO-identical transplant, and 357 (60.8%) received ABO-mismatched transplants, including 161 (27.4%) minor, 141 (24.0%) major, and 55 (9.4%) bidirectional ABO-incompatible UCBTs. All patients received myeloablative conditioning regimens and cyclosporine A (CsA) combined with mycophenolate mofetil (MMF) as a GVHD prophylaxis. Results A comparison of ABO compatibility and incompatibility demonstrated no significant differences (P>0.05) in the cumulative incidence of neutrophil, platelet, and red blood cell engraftment . There was no significant difference in the cumulative incidence of grades Ⅱ to Ⅳ aGVHD (P= .527) and Ⅲ to Ⅳ aGVHD (P= .949) among the 4 groups (Figure A , B). In univariate analysis, ABO blood group incompatibility was not associated with cumulative incidence of 180d TRM (Figure C, P= .602). The overall 3-year survival had no statistically significant differences among the 4 groups (Figure D; P= .384). Further, 11 patients were excluded from the analysis of post-UCBT RBC transfusion burden because of missing data and non-red blood cell engraftment. Of the remaining 576 patients, the median number of RBC transfusions during transplant days 0 to 60 was 4 (range, 0 to 106). There was no significant difference in the transfusion burden among all ABO blood type mismatch groups (Table 1, P = .069). Furthermore, none of the patients developed pure red aplastic anemia (PRCA) after UCBT. Conclusion The results showed that ABO blood group incompatibility had no significant impact on hematologic engraftment, the occurrence of GVHD, and the survival of malignant hemoblastosis. Patients with myeloablative single-unit UCBT may not develop PRCA; Donor-recipient ABO incompatibility may not be the major consideration in the selection of umbilical cord blood. Disclosures No relevant conflicts of interest to declare.
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Kahwaji, Joseph, Ashley A. Vo, and Stanley C. Jordan. "ABO blood group incompatibility: a diminishing barrier to successful kidney transplantation?" Expert Review of Clinical Immunology 6, no. 6 (November 2010): 893–900. http://dx.doi.org/10.1586/eci.10.78.

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Maria Elfving, A., Bengt A. Lindberg, M. Landin-Olsson, Christine S. Hampe, Åke Lernmark, and Sten-A. Ivarsson. "Islet Cell Autoantibodies in Cord Blood from Children with Blood Group Incompatibility or Hyperbilirubinemia." Autoimmunity 36, no. 2 (January 2003): 111–15. http://dx.doi.org/10.1080/0891693031000073109.

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Tsuji, Masanori, Atsushi Wake, Naoyuki Uchida, Kazuya Ishiwata, Nobuaki Nakano, Shinsuke Takagi, Hisashi Yamamoto, et al. "Impact of ABO Imcompatibility On Acute GvHD and Thrombotic Microangiopathy After Reduced-Intensity Cord Blood Transplantation." Blood 114, no. 22 (November 20, 2009): 2298. http://dx.doi.org/10.1182/blood.v114.22.2298.2298.

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Abstract Abstract 2298 Poster Board II-275 Introduction: Althouth ABO blood type is one of two antigen system for transplantation, the effect of ABO incompatibility on transplantation outcome still remains controversy. Furthermore, there is little data about ABO incompatibility on the outcome of unrelated cord blood transplantation following reduced-intensity conditioning (RI-CBT). Design and Methods: We retrospectively analyzed data of 155 patients who underwent RI-CBT performed at Toranomon Hospital from January 2005 to December 2008. The patients include 45 ABO-identical, 47 minor, 43 major, and 20 bidirectional ABO mismatched. All patients were performed using fludarabine-based reduced-intensity conditioning, and 114 patients (74%) were performed using TBI-containing regimen. Median age were 57 years-old and 94 patients (61%) were over 55 years-old. We evaluated the association between ABO incompatibility and neutrophil engraftment, one-year overall survival (OS) ; one-year non-relapsed mortality (NRM) ; and one-year relapse rate. We also analyzed the incidence of pre-engraftment immune reaction (PIR), acute graft-versus-host disease (GvHD) including severity, and thrombotic microangiopathy (TMA). Results: There were no significant differences in neutrophil-engraftment time, reticulocyte-engraftment time, and the incidence of PIR. The incidence of acute GvHD and grade 2-4 acute GvHD were significantly higher in major/bidirectional ABO-incompatible group than ABO-identical/minor ABO-incompatible group (respectively P=0.0008 and P=0.0116). The incidence of TMA tended to be higher in minor/bidirectional ABO-incompatible group than ABO-identical/major ABO-incompatible group (P=0.0637). There were no significant differences in one-year OS, NRM, and relapse rate. In multivariate analysis, risk factors of acute GvHD were age over 55, TBI-containing regimen, CD34-positive cells>0.7×10e5/kg, and major/bi-directional ABO incompatibility, and those of TMA were grade 3-4 acute GvHD and minor/bi-directional ABO incompatibility. Discussion: This study showed major-directional ABO incompatibility setting increased the incidence of acute GvHD. Sex incompatibility and HLA incompatibility were not significantly influenced the incidence of acute GvHD. The use of steroid for severe GvHD and the expression of ABO antigen on the surface of vascular endothelial cell may influence pathogenesis of TMA. Further studies including larger patients numbers are required to elucidate the impact of ABO incompatibility on the clinical outcome of RI-CBT. Disclosures: No relevant conflicts of interest to declare.
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Obukhova, P. S., A. V. Kachanov, N. A. Pozdnyakova, and M. M. Ziganshina. "AB0-incompatibility of mother and fetus: the role of anti-glycan alloantibodies in the hemolytic disease of newborns." Medical Immunology (Russia) 23, no. 1 (March 1, 2021): 17–34. http://dx.doi.org/10.15789/1563-0625-aom-1977.

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The mother and fetus incompatibility due to Rh-factor, blood group or other blood factors can lead to hemolytic disease of the fetus and newborn (HDN). HDN is a clinical disease condition of the fetus and newborn as a result of hemolysis, when maternal IgG alloantibodies cross the placenta and destroy the red blood cells of the fetus and newborn. The child disease begins in utero and can dramatically increase immediately after birth. As a result, hyperbilirubinemia and anemia develop, that can lead to abortions, serious complications, or death of the neonates in the absence of proper therapy. The range of HDN has changed significantly now compared to previous decades. Half a century ago, HDN was considered an almost complete synonym of RhD-alloimmunization, and this was a frequent problem for newborns. By now due to the high effective of Rh-conflict prevention, immunological AB0-conflicts have become the most common cause of HDN. The review aimes to one of the main causes of jaundice and anemia in neonates at present, i.e. HDN due to immunological AB0-conflict of mother and newborn (AB0-HDN). The main participants of the AВ0- incompatibility mother and child are considered, namely A- and B-glycans, as well as the corresponding anti-glycan alloantibodies. Close attention is paid to the structure features of glycan alloantigens on the red blood cells of the fetus and adult. The possible correlation of the frequency and severity of HDN with the blood group of mother and child, as well as with the titer of maternal alloantibodies, has been considered. The influence of immunoglobulin G subclasses on the AB0-HDN development has been evaluated. In most cases, AB0-HDN appear when the mother has the blood group 0, and the fetus has the group A (subgroup A1) or the group B. Other rare incidences of AB0-incompatibility with severe course are occurred. As a whole the etiology of AB0-HDN is complex and the HDN severity is influenced by many factors. The authors have analyzed statistical data, as well as the prevalence of AB0-incompatibility and AB0-HDN in various regions of the world. Current approaches to the diagnosis of AB0-HDN are discussed in addition. By now the problems of AB0- HDN occurrence and developing of ways to overcome this disease remain relevant.
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Curtis, Brian R., Janice G. McFarland, Andrea Fick, Andrew J. Lochowicz, Robert H. Ball, and Aster H. Richard. "Neonatal Alloimmune Thrombocytopenia (NATP) Associated with Maternal-Fetal Incompatibility for Blood Group B." Blood 106, no. 11 (November 16, 2005): 955. http://dx.doi.org/10.1182/blood.v106.11.955.955.

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Abstract In most individuals, A and B blood group antigens are weakly expressed on platelets, allowing ABO incompatible platelets to be tolerated when transfused. However, in a minority of normal subjects (high expressers, H-Exp), platelets carry 10–20 times the usual number of A or B epitopes (up to 20,000/platelet, Blood2000;96:1574). Post-transfusion survival of incompatible H-Exp platelets has not been systematically studied. We recently encountered a family in which NATP in two infants appears to have been caused by maternal anti-B reacting with H-Exp fetal platelets inherited from a father with the group B H-Exp trait. The first two children (C1 and C2) born to a G4P2 group O mother and A2B father were positive for blood group B, and had neonatal thrombocytopenia (TP) (C1 = 33K/μL, C2 = 61K/μL), anemia, positive direct antiglobulin test, elevated reticuloytes and hyperbilirubinemia requiring phototherapy. C1 required 3 platelet transfusions and RBC transfusion, and C2 required RBC transfusion. Both recovered in the immediate neonatal period. A third child (C3) inherited blood group A2 from the father and was born with a normal platelet count. The parents were incompatible for HPA-2b and -3b, but no platelet-specific antibodies were detected in maternal serum. High titer IgG antibodies were detected in maternal serum against father’s platelets in both flow cytometry and modified antigen capture ELISA. This activity was completely removed by absorption with normal, washed group B RBCs. When tested by flow cytometry with monoclonal anti-B and anti-A, the father’s platelets were shown to carry 17 times the normal level of B antigen, and only trace amounts of A antigen. We previously showed that the potent glycosyltransferase activity associated with the H-Exp trait causes essentially all H antigen on platelets and RBCs to be converted to A and/or B antigen. Consistent with this, father’s platelets and RBCs were found to express no detectable H. Quantitation of B and H antigens on platelets and RBCs from C1 and C2 is pending receipt of samples. Findings made in this family indicate that maternal anti-B (and presumably anti-A) IgG antibodies can cause NATP in infants with the ABO “high expresser” trait. Maternal-fetal ABO incompatibility should be considered as a cause of NATP when maternal antibodies against platelet-specific antigens cannot be demonstrated. The possibility that ABO incompatibility can aggravate thrombocytopenia caused by antibodies against recognized platelet-specific antigens also deserves consideration.
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Rao, Latha B., Zohaib Ahmed, and Bulent Ozgonenel. "The Clinical Spectrum of ABO Incompatibility and Hemolytic Disease in the Newborn." Blood 120, no. 21 (November 16, 2012): 1182. http://dx.doi.org/10.1182/blood.v120.21.1182.1182.

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Abstract Abstract 1182 Introduction: ABO hemolytic disease of the newborn occurs almost exclusively in infants of blood group A or B who are born to group O mothers. Although ABO incompatibility is common, its related hemolytic disease has been reported to be low. In this study, we aimed to investigate the rate of direct anti-globulin test (DAT) positivity and clinical events, such as hyperbilirubinemia or anemia in infants born to group O mothers. Methods: Using the charge code for cord blood evaluation, we were able to identify all cord blood evaluations from January 1, 2006 - December 31, 2007, and then select out the ABO incompatible births from group O mothers. We then reviewed the electronic medical records for demographic, clinical and laboratory information. Clinical events (anemia, jaundice, hemolytic disease) were investigated only in babies born at 37 weeks or higher gestation. Chi-square tests were used to cross-tabulate clinical events, demographic parameters (gender, ethnicity), and laboratory parameters (AO versus BO incompatibility, DAT-positivity). Results: There were 10,891 live births during the two-year period and 1519 (14%) of these were ABO incompatible. ‘Black’ ethnicity was registered in 80% of these babies. AO and BO incompatibility comprised 57.8% and 42.2% of the cases, respectively. 5.3% of the cases had concomitant Rh incompatibility. DAT was positive in 16.7% of the cases: 13.8% weakly or 1+ positive, and 2.9% 2+ or 3+ positive. DAT was more commonly positive among BO-incompatible cases compared to AO-incompatible cases (21.7% versus 13.1%). Among blacks, DAT-positivity in BO incompatibility was more common (24.9% among blacks compared to 7.8% among non-blacks, p<0.001). Concomitant Rh incompatibility did not affect DAT positivity rate. Among AO-incompatible babies, DAT-positivity was more frequent among females (15.5% in females vs 10.8% in males, p=0.045). 1299 babies were born at term (3 37 weeks gestation).of these infants, hyperbilirubinemia (defined as indirect bilirubin 3 8 mg/dL) was detected in 17.3% of babies. This was significantly associated with DAT positivity (40.6% in DAT-positive cases vs 12.3% in DAT-negative cases, p<0.001) and BO incompatibility (p=0.001). Hemolytic anemia (defined as hematocrit £ 45% and reticulocyte count 3 250,000/mm3 in the first week of life) was noted in 3.4% of cases, and was significantly associated with DAT positivity (13.2% in DAT-positive cases vs 1.1% in DAT-negative cases, p<0.001); BO incompatibility (p=0.001); and black ethnicity (p=0.001). Discussion: Our study indicated that cord blood DAT was positive in 16.7% of ABO incompatible pregnancies. BO-incompatible cases were more likely to be DAT-positive in blacks. AO-incompatibility was more common among girls, consistent with earlier studies that had shown a stronger A antigen expression among female newborns. DAT-positive cases were more likely to develop hyperbilirubinemia or hemolytic anemia. In addition, black ethnicity and BO incompatibility conferred significantly increased risk of hemolytic anemia in our study. Despite this strong association, the sensitivity of the positive DAT was 41.3% for hyperbilirubinemia and 70.5% for hemolytic anemia in ABO incompatibility. Disclosures: No relevant conflicts of interest to declare.
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Chen, Yang, Huiru Wang, Zimin Sun, Wen Yao, Huilan Liu, Xiaoyu Zhu, and Dongyao Wang. "Abo不相容性和抗a / B异凝集素滴度对血液恶性肿瘤清髓处理后输血需求和无关脐带血移植的早期结果的影响." Blood 136, Supplement 1 (November 5, 2020): 26. http://dx.doi.org/10.1182/blood-2020-143297.

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Abstract Background:ABO incompatibility is not considered a main contraindication to allogeneic hematopoietic stem cell transplantation (aHSCT). However, it has been associated with a number of immunohematological complications. The effects of ABO incompatibility on aHSCT remain controversial.The change of isoagglutinin titers and early clinical outcomes were analyzed after unrelated cord blood transplantation (UCBT) with ABO-incompatibility donor. Methods:252 patients with hematological malignant diseases and other hematological disorders who underwent unrelated UCBT from January 2019 to April 2020 were retrospectively analyzed in this research. Patients were studied in identical, major, minor and bidirectional mismatch groups. Immunoglobulin m (IgM) isoagglutinin titers were tested one day before the transplant (-1 day), 2 weeks post-transplant, 4 weeks post-transplant and 6 weeks post-transplant. R esults:76 match,71 major mismatch, 70 minor mismatch and 35 bidirectional unrelated UCBT were identified. The median neutrophil, PLT and red blood cell (RBC) recovery days were 18, 38 and 22, respectively. ABO mismatch did not influence the neutrophil, PLT and RBC engraftment. The median of RBC transfusion in 30 days were 5 units and PLT were 6 units. There were no statisitcal difference in 0-30 days RBC and PLT transfusion after UCBT. 31-100 days transfusion was similar to in 30 days transfusion. No patients developed pure red cell anemia (PRCA). -1day IgM titers ≥1:16 did not develop higher risk of grade II-IV aGVHD when compared with titers≤1:8 group. However, we detected a marginal higher PLT transfusion in 30 days after transplant at antibody titers ≥1:16 group when compared with titers≤1:8 (P=0.051). In the major and bidirectional groups, we found that group O IgM anti-donor antibodies were displayed a significant higher than the group B anti-A titer (p&lt;0.001) in setting the time one day before the transplant, but no significant with group A. 2 weeks after the transplant, group B anti-A was still showed significant lower than the group O anti-A (p&lt;0.001). 4 weeks after the UCBT, we observed a modest, but no statistical significant lower titers of group B anti-A antibodies as compared with O group (P=0.097). 6 weeks after the transplant, there were no statistical significant among group O, A and B. In the multivariable Cox regression model, transfusion of ≥5 RBC units in 30 days after UCBT (HR=1.727, 95%CI=1.020-2.926, P=0.042) and PLT engraftment ≥38 days (HR=1.964, 95%CI=1.134-3.401, P=0.016) were correlated to greater risk of grade severe aGVHD. Conclusion:This study showed that ABO mismatch did not influence the neutrophil, PLT and RBC recovery time.Group O IgM anti-donor isoagglutinins in recepients showed a higher titers than the group B in setting with the time (-1 days pre-transplant, 2 weeks post-transplant, 4 weeks post-transpant). Pre-transplant higher anti-donor isoagglutinins were associated with more PLT transfusion requirements after UCBT. More RBC transfusion (≥5 units) and longer PLT recovery time (≥38 days) showed a higher incidence of severe aGVHD. Disclosures No relevant conflicts of interest to declare.
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Yoshida, H., K. Ito, T. Kusakari, K. Ida, Y. Ihara, T. Mori, and M. Matsumura. "Removal of maternal antibodies from a woman with repeated fetal loss due to P blood group incompatibility." Transfusion 34, no. 8 (August 1994): 702–5. http://dx.doi.org/10.1046/j.1537-2995.1994.34894353467.x.

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Dissertations / Theses on the topic "Blood Group Incompatibility – immunology"

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Kandeva, Teodora N. 1983. "Humoral response to carbohydrate antigens in the context of ABO-incompatible transplantation and xenotransplantation." Thesis, McGill University, 2008. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=116121.

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Antibody-mediated rejection is central to ABO incompatible transplantation as well as to xenotransplantation. The xenoantigen alpha-Gal has a highly analogous carbohydrate structure to the human blood group antigens, and both require memory B cell activation for antibody production. We hypothesize that B cells, reactive to the alpha-Gal xenoantigen and B blood group antigen, require the presence of fully activated T cells in order to survive and proliferate in vitro, contrary to the traditional theory that humoral response to carbohydrate antigens is a T cell-independent process. When we compared the capacity of B cells to proliferate, we observed that activated T cells were necessary for B cell proliferation even in the presence of carbohydrate-derived antigens. A relevant question was also to investigate the role of a specific class of T cells: the CD1d-restricted iNKT cells, in the activation of alpha-Gal and B blood group-reactive B cells. The iNKT cells have the specificity of being reactive to glycolipids and are capable of producing both T helper 1 and T helper 2 cytokine responses. We therefore wanted to determine the role of the iNKT cells as mediators of a T helper 2-type response when B cells were exposed to a glycolipid antigen expressing the alpha-Gal epitope or the human B blood group antigen. We observed that, if the interaction between B cells and iNKT cells is blocked, neither B cell proliferation nor antibody production occurs. These results suggest therefore the importance of the iNKT cell category of T helper cells in the response to alpha-Gal and ABO-blood group glycolipids.
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Santis, Laís Priscila de. "Análise proteômica na caracterização de anticorpos monoclonais dirigidos contra antígenos eritrocitários e leucocitários humanos." Botucatu, 2018. http://hdl.handle.net/11449/154883.

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Orientador: Andrei Moroz
Resumo: As membranas de hemácias e leucócitos são compostas por centenas de antígenos que desempenham diversas funções relacionadas a homeostase, metabolismo celular e podem estar envolvidos em processos de rejeição de transplantes, doenças hemolíticas e reações transfusionais. Para a detecção desses antígenos são utilizados anticorpos monoclonais e a obtenção destes anticorpos envolve diversas etapas que culminam na caracterização dos produtos obtidos. Esta etapa é crítica e envolve diferentes técnicas, incluindo a Proteômica na descrição da proteína-alvo de cada anticorpo monoclonal. O objetivo deste estudo foi caracterizar anticorpos monoclonais de especificidade anti-eritrocitária e anti-leucocitária produzidos pelo Laboratório de Engenharia Celular (LEC) do Hemocentro de Botucatu. Foram selecionados um clone e um hibridoma produtores de anticorpos anti-eritrocitários, e um clone produtor de anticorpos anti-leucocitários, pertencentes ao banco de células do LEC. As células foram expandidas em cultura, foi realizado Western Blotting (WB) e cada banda proteica reconhecida pelos anticorpos (antígenos) foi analisada por Espectrometria de Massas, segundo técnicas proteômicas. Outros testes adicionais foram realizados, como técnicas imuno-hematológicas, citometria de fluxo e imuno-histoquímica. Após expansão, retestagem e verificação de reatividade contra hemácias humanas, e a seleção dos dados de outros estudos até então não explorados, na técnica de WB os anticorpos reconheceram dive... (Resumo completo, clicar acesso eletrônico abaixo)
Abstract: Red blood cell and leukocyte membranes are composed of hundreds of antigens that perform various functions related to homeostasis, cell metabolism and may be involved in transplant rejection, hemolytic disease and transfusion reactions. Monoclonal antibodies are used to detect these antigens and the obtaining of these antibodies involves several steps that culminate in the characterization of the obtained products. This step is critical and involves different techniques, including Proteomics to descript the target protein of each monoclonal antibody. The aim of this study was to characterize anti-erythrocyte and anti-leukocyte monoclonal antibodies produced by the Laboratory of Cellular Engineering (LEC) of the Blood Center of Botucatu. Anti-erythrocytes clone and hybridoma antibody producers and a clone that produces anti-leukocyte antibodies, belonging to the LEC cell bank were selected. Cells were expanded in culture, it was realyzed Western Blotting (WB) technique and each protein band recognized by the antibodies (antigens) was analyzed by Mass Spectrometry according to proteomic techniques. Others tests were realized, such as immunohematology techniques, flow cytometry and immunohistochemistry. After expansion, retesting and verification of reactivity against human red blood cells, and selection of data from other studies not exploited, in the WB technique, the antibodies recognized several spots. After analysis by Mass Spectrometry, it was identified, with good reliabi... (Complete abstract click electronic access below)
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Amaral, Daphne Renata Tavares. "Determinação do genótipo RHD fetal através do plasma materno em gestantes RhD-negativo de uma população do Brasil." [s.n.], 2010. http://repositorio.unicamp.br/jspui/handle/REPOSIP/310413.

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Orientador: Lilian Maria de Castilho
Dissertação (mestrado) - Universidade Estadual de Campinas, Faculdade de Ciências Médicas
Made available in DSpace on 2018-08-16T19:56:37Z (GMT). No. of bitstreams: 1 Amaral_DaphneRenataTavares_M.pdf: 1431812 bytes, checksum: 82f80c8b6c347220a22a8345ee9be187 (MD5) Previous issue date: 2010
Resumo: A análise de plasma materno para a determinação do genótipo RHD fetal é uma importante ferramenta no acompanhamento de gestantes RhD-negativo, especialmente em pacientes aloimunizadas. Este trabalho verificou a acurácia da genotipagem RHD fetal pela análise do plasma materno em uma população do Brasil. Foram analisadas 88 gestantes RhD-negativo entre 11 e 39 semanas de gestação, com idade mediana de 28 anos. Treze (14,78%) pacientes encontravam-se aloimunizadas com anti-D. Foram utilizados primers e sondas para detecção do gene RHD (exons 4, 5 e 10) por PCR em tempo real. Como controle interno, utilizou-se um conjunto de primers e sondas para identificar o genes SRY e CCR5. Sangue periférico ou sangue de cordão umbilical dos respectivos neonatos foram coletados durante o parto para a realização da fenotipagem RhD. A genotipagem RHD convencional foi realizada em todas as 88 amostras de DNA materno. Oitenta e três (94,32%) gestantes apresentaram a deleção do gene RHD e em 5 (5,68%) amostras foram identificadas variantes do gene RHD (3 RHD e 2 DFR). A genotipagem RHD convencional foi também realizada em 17 amostras de DNA paternas. Quinze amostras (88,24%) foram genotipadas como RHD+ (5 RHD+/RHD+ e 10 RHD+/RHD-) e 2 (11,76%), como RHD-. Cinqüenta e oito (65,91%) fetos foram genotipados como RHD+. Vinte e sete (30,68%) amostras apresentaram ausência completa do gene RHD e três fetos apresentaram amplificação apenas para o exon 10, demonstrando a presença de uma possível variante RHD ou RHD-CE-Ds. Todos os resultados da genotipagem RHD fetal foram concordantes com a fenotipagem neonatal incluindo os 3 fetos com a variante RHD, fenotipados como RhD-. Nossos resultados indicam que a genotipagem RHD fetal através da análise do plasma materno amplificando 3 regiões do gene RHD (exons 4, 5 e 10) é adequada para a aplicação clínica. Este protocolo pode-se tornar prática em um futuro próximo
Abstract: Maternal plasma analysis for determination of the fetal RHD status is an important tool for the management of RhD-negative pregnant, specially alloimunized women. We assessed the accuracy of fetal RHD genotyping by analysis of maternal plasma in a multi-ethnic population. We analyzed plasma samples from 88 RhD-negative pregnant women between 11 and 39 weeks of gestation, median age of 28 years old to determine the fetal RHD genotype. This population was from Southeastern Brazil with high mixed ethnic background. Thirteen patients (14,78%) had anti-D alloantibody. We used TaqMan primers and probes to detect exons 4, 5 and 10 of RHD, by real-time PCR. As internal controls, we used primers/probes sets to SRY and CCR5. Peripheral or umbilical cord bloods from respective neonates were collected during delivery and hemagglutination was performed. Conventional RHD genotyping was realized in all pregnant. Eighty-three patients had a deletion of RHD gene and five samples were identified RHD variants (3 RHD and 2 DFR). The conventional RHD genotyping was also performed on 17 DNA samples from fathers. Fifteen samples were genotyped as RHD+ (5 RHD+/RHD+ and 10 RHD+/RHD-) and 2 RHD-negative. Fifty-eight (65,91%) fetuses were genotyped as RHD+. Twenty-seven (30,68%) samples showed completely absence of RHD and three fetuses showed amplification only for the exon 10, demonstrating the presence of a possible variant (RHD or RHD-CE-Ds). All fetal RHD results agreed with the neonatal typing including the 3 fetuses with RHD variant, phenotyped as RhD-negative. Thus, the accuracy of the fetal RHD genotyping in this population was 100%. The earliest pregnancy in which fetal RHD was detected was 11 weeks. Our findings indicate that the accuracy of fetal RHD genotyping from maternal plasma using 3 regions (exons 4, 5 and 10) can be sufficient for clinical application in a multi-ethnic population. This knowledge helped us on the development of a feasible protocol for fetal RHD genotyping on DNA from maternal plasma in our population and should become practice in the near future
Mestrado
Ciencias Basicas
Mestre em Clinica Medica
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Baker, Patrick Ericson. "Genetic regulation of virulence factors contributing to colonization and pathogenesis of helicobacter pylori." The Ohio State University, 2003. http://rave.ohiolink.edu/etdc/view?acc_num=osu1061414659.

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Books on the topic "Blood Group Incompatibility – immunology"

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Takahashi, Kōta. ABO-incompatible kidney transplantation. New York: Elsevier, 2001.

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Christine, Lomas-Francis, ed. The blood group antigen: Factsbook. 2nd ed. London: Academic Press, 2004.

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Popovsky, Mark A. Transfusion reactions. 4th ed. Bethesda, Md: AABB Press, 2012.

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Reid, Marion E. The blood group antigen factsbook. 2nd ed. Amsterdam: Elsevier/Academic Press, 2003.

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Christine, Lomas-Francis, ed. The blood group antigen factsbook. San Diego: Academic Press, 1997.

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T, Johnson Susan, Storry Jill, Judd W. John, and American Association of Blood Banks., eds. Judd's methods in immunohematology. 3rd ed. Bethesda, MD: AABB Press, 2008.

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Clinical immunohematology: Basic concepts and clinical applications. Boston: Blackwell Scientific Publications, 1990.

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Schenkel-Brunner, Helmut. Human blood groups: Chemical and biochemical basis of antigen specificity. 2nd ed. Wien: Springer, 2000.

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Schenkel-Brunner, Helmut. Human blood groups: Chemical and biochemical basis of antigen specificity. Wien: Springer-Verlag, 1995.

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Reid, Marion E. Blood group antigens and antibodies: A guide to clinical relevance & technical tips. New York: Star Bright Books, 2007.

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Book chapters on the topic "Blood Group Incompatibility – immunology"

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Ajmani, Pritam Singh. "Blood Group and Immunology." In Immunohematology and Blood banking, 7–23. Singapore: Springer Singapore, 2020. http://dx.doi.org/10.1007/978-981-15-8435-0_2.

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Lundblad, Arne, and M. Alan Chester. "Blood Group Active Haptens in Urine and Faeces." In The Molecular Immunology of Complex Carbohydrates, 73–81. Boston, MA: Springer US, 1988. http://dx.doi.org/10.1007/978-1-4613-1663-3_3.

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Hansson, Gunnar C. "Structural Aspects of Blood Group Glycosphingolipids in the Gastrointestinal Tract." In The Molecular Immunology of Complex Carbohydrates, 465–94. Boston, MA: Springer US, 1988. http://dx.doi.org/10.1007/978-1-4613-1663-3_17.

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Anderson, Byron, Lyman E. Davis, and Mario Venegas. "Tumor-Associated Blood Group Antigen Expressions and Immunoglobulins Associated with Tumors." In The Molecular Immunology of Complex Carbohydrates, 601–56. Boston, MA: Springer US, 1988. http://dx.doi.org/10.1007/978-1-4613-1663-3_25.

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Watkins, W. M. "Blood Group Antigens and the Enzymes Involved in their Synthesis: Past and Present." In The Molecular Immunology of Complex Carbohydrates, 349–50. Boston, MA: Springer US, 1988. http://dx.doi.org/10.1007/978-1-4613-1663-3_13.

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Laine, Roger A., and Jeffrey S. Rush. "Chemistry of Human Erythrocyte Polylactosamine Glycopeptides (Erythroglycans) as Related to ABH Blood Group Antigenic Determinants." In The Molecular Immunology of Complex Carbohydrates, 331–47. Boston, MA: Springer US, 1988. http://dx.doi.org/10.1007/978-1-4613-1663-3_12.

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Wu, Albert M. "Structural Concepts of the Human Blood Group A, B, H, Lea, Leb, I and i Active Glycoproteins Purified from Human Ovarian Cyst Fluid." In The Molecular Immunology of Complex Carbohydrates, 351–94. Boston, MA: Springer US, 1988. http://dx.doi.org/10.1007/978-1-4613-1663-3_14.

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Lubenko, Anatole, and Marcela Contreras. "ABO Blood Group System." In Encyclopedia of Immunology, 1–5. Elsevier, 1998. http://dx.doi.org/10.1006/rwei.1999.0001.

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Löw, Bengt. "Blood group serology for clinical use." In Immunology, 253–59. Elsevier, 1985. http://dx.doi.org/10.1016/b978-0-407-00372-9.50027-4.

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Cooper, Chris. "6. Blood transfusion." In Blood: A Very Short Introduction, 103–23. Oxford University Press, 2016. http://dx.doi.org/10.1093/actrade/9780199581450.003.0006.

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Abstract:
‘Blood transfusion’ outlines the history of transfusing animal blood dating back to the 17th century. The 19th century saw the first successful human blood transfusion, but two major issues remained: the problems of clotting and blood group incompatibility. Albert Hustin and Luis Agote resolved the first issue in 1914 by using sodium citrate in transfusions to work as an anticoagulant. Richard Lewisohn calculated the correct levels of citrate needed to avoid poisoning the blood. Karl Landsteiner’s work in early 20th-century Vienna revealed the ABO blood type distinctions, solving the latter problem. The creation of blood banks and the potential for viral contamination of blood and blood products are also discussed.
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