Academic literature on the topic 'Alloantigens'
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Journal articles on the topic "Alloantigens"
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Owens, T., and I. N. Crispe. "Suppressor T cells, distinct from "veto cells," are induced by alloantigen priming and mediate transferable suppression of cytotoxic T lymphocyte responses in vivo." Journal of Immunology 135, no. 5 (1985): 2984–89. http://dx.doi.org/10.4049/jimmunol.135.5.2984.
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Abstract Primary and secondary cytotoxic T lymphocyte responses to minor alloantigens can be suppressed by priming host mice with a high dose (10(8) cells) of alloantigenic donor spleen cells (SC). Such suppression is antigen specific and transferable into secondary hosts with T cells. One interpretation of this is that antigen-specific host suppressor T cells (Ts) are activated. Alternatively, donor Lyt-2+ T cells, introduced in the priming inoculum, may inactivate host CTL precursors (CTLp) that recognize the priming (donor) alloantigens. Donor cells that act in this way are termed veto T cells. The experiments described here exclude veto T cell participation in transferable alloantigen-specific suppression, and demonstrate the operation of an alloantigen-specific host-derived T suppressor (Ts) cell. The origin of the Ts has been studied directly by using Thy-1-disparate BALB/c mice. The cell responsible for the transfer of suppression of a secondary CTL response to B10 minors was of the host Thy-1 allotype, and so originated in the host spleen and was not introduced in the priming inoculum. Secondly, antigen-specific Ts generated in CBA female mice against B10 minors could act on CTL responses to an unequivocally non-cross-reactive-third party antigen (H-Y), provided the two antigens were expressed on the same cell membrane. Such third-party suppression is incompatible with the operation of veto T cells. Depletion of Thy-1.2+ or Lyt-2+ cells from the suppression-inducing donor SC inoculum did not abrogate suppression induction in BALB/c mice; instead, suppression was enhanced. The demonstration of veto cell activity in similarly primed mice by other groups of investigators indicates that both types of suppression may operate. However, our results show that only antigen-specific Ts can mediate the transferable suppression of CTL responses to alloantigens.
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Chen, Benny J., Divino Deoliveira, Xiuyu Cui, et al. "Inability of memory T cells to induce graft-versus-host disease is a result of an abortive alloresponse." Blood 109, no. 7 (2006): 3115–23. http://dx.doi.org/10.1182/blood-2006-04-016410.
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Abstract Several groups, including our own, have independently demonstrated that effector memory T cells from non–alloantigen-primed donors do not cause graft-versus-host disease (GVHD). In the current study, we further investigated whether this approach could be extended to all memory T cells, and we studied the underlying mechanisms. Neither total memory T cells nor purified central memory T cells were able to induce GVHD. Memory T cells were at least 3-log less potent than bulk T cells in mediating GVHD. As expected, memory T cells failed to elicit cytotoxicity and proliferated poorly against alloantigens in standard 5-day mixed-lymphocyte cultures. However, the proliferative responses of memory T cells were more comparable with those of bulk and naive T cells when the culture time was shortened. Moreover, the frequencies of IL-2–secreting cells measured by 42-hour enzyme-linked immunosorbent spot (ELISPOT) assay were similar among naive, memory, and bulk T cells. These data indicated that memory T cells are able to respond to alloantigens initially but fail to develop to full potential. The abortive immune response, which was mediated by non–alloantigen-specific memory T cells in response to alloantigens, may explain why memory T cells from unprimed and non–alloantigen-primed donors could not induce GVHD.
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Patel, Seema R., Ashley Bennett, Kathryn Girard-Pierce, et al. "Recipient priming to one RBC alloantigen directly enhances subsequent alloimmunization in mice." Blood Advances 2, no. 2 (2018): 105–15. http://dx.doi.org/10.1182/bloodadvances.2017010124.
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Key Points CD4+ T cells primed to one RBC alloantigen promote humoral immunity to a disparate RBC alloantigen when both antigens are on the same RBC. These findings provide a potential explanation for how responses to one antigen may enhance antibody formation to other RBC alloantigens.
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Bianchi, A. T., M. W. Schilham, R. Benner, P. Young, and I. Lefkovits. "In vivo priming of helper and suppressor T cells by alloantigens. Frequency analysis with the use of an in vitro limiting dilution assay." Journal of Immunology 139, no. 8 (1987): 2524–29. http://dx.doi.org/10.4049/jimmunol.139.8.2524.
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Abstract Earlier studies have demonstrated that T cells activated in mixed lymphocyte reactions can exert positive as well as negative allogeneic effects on B cells expressing the appropriate alloantigens on their surface. We investigated the effect of in vivo priming of T cells with alloantigens on their capacity to help or suppress allogeneic B cell cultures against sheep erythrocytes. We used immunization protocols that have been shown to be optimal for induction of alloantigen-specific delayed-type hypersensitivity (DTH) and alloantigen-specific suppressor T (Ts) cells for DTH. The results show that in vivo stimulation with alloantigens, depending on the immunization route and the lymphoid organ studied, can be as effective as in vitro stimulation in increasing the frequency of alloantigen-specific helper T (Th) cells and Ts cells. Subcutaneous immunization induced a 10-fold frequency raise of Th cells as well as of Ts cells in the lymph nodes. In the spleen the Th cell population was hardly affected by s.c. immunization, whereas the Ts cell population increased by at least a factor 20. Intravenous immunization, on the other hand, selectively expanded the Th cell population in the spleen, whereas the splenic Ts cell population and the Th and Ts cells in the lymph nodes were not affected. Comparison of these results with our previous data concerning characteristics and the requirements of in vivo activation of alloantigen-specific DTH reactive T cells and of alloantigen-specific Ts cells suggest that different Ts cell populations are involved in suppression of alloantigen-specific DTH in vivo and of allogeneic suppression of in vitro induced sheep erythrocytes specific antibody formation.
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Schadendorf, D., H. Yamaguchi, L. J. Old, and P. K. Srivastava. "A novel heteromorphic human cell surface alloantigen, gp60, defined by a human monoclonal antibody." Journal of Immunology 142, no. 5 (1989): 1621–25. http://dx.doi.org/10.4049/jimmunol.142.5.1621.
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Abstract A human mAb (DSM1) generated from a patient immunized with irradiated allogeneic melanoma cells detects a new cell surface alloantigen of restricted cell type distribution. The Ag is a 60,000-Da glycoprotein (gp60) that displays considerable heteromorphism in its cytosolic and cytoskeletal (52 to 62 kDa) and membrane forms (60 to 64 kDa). The gp60 Ag has been purified using lectin affinity, ion exchange, and Mono P fast performance liquid chromatography. Rabbit antiserum against purified gp60 recognizes a homologous gp60 molecule on DSM1-nonreactive cells. Molecular properties of gp60 and a partial amino acid sequence of a tryptic gp60-derived peptide distinguish it from other known human alloantigens. This is the first report of a human alloantigenic system whose definition required a cell type other than those of bone marrow derivation.
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Isakov, N., and F. H. Bach. "Participation of class II alloantigens in in vivo regulation of K/D region disparate thyroid graft rejection in mice." Journal of Immunology 134, no. 6 (1985): 3580–85. http://dx.doi.org/10.4049/jimmunol.134.6.3580.
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Abstract Class I and II molecules preferentially activate cytotoxic T cells and helper T cells, respectively, in primary in vitro alloactivation of T lymphocytes. Collaboration between these subpopulations leads to an efficient anti-class I specific cytotoxic response. We tested whether the presence of class II, in addition to class I, alloantigens on thyroid allografts in vivo induces augmentation of anti-class I antigen immune response and leads to rejection of K/D region disparate grafts which otherwise would have been accepted. Different pairs of K or D region disparate mouse strains were selected in which transplantation across a class I antigen disparity alone resulted in long-term graft acceptance. In some pairs of mouse strains, co-transplantation of recipient mice with a second thyroid graft sharing the K/D region of the first, but additionally expressing an allo class II molecule, led to accelerated K/D region disparate thyroid graft rejection. Transplantation of thyroid allografts expressing both class II and I alloantigens did not induce increased host anti-class I antigen cytotoxic response, or affect the frequency of specific precursor cytotoxic T cells. In one pair of congenic mouse strains, acute rejection of K/D region disparate thyroid grafts occurred in the absence of class II alloantigen stimulation; in other strains, co-transplantation of class I and II alloantigen disparate thyroid allografts was not sufficient to induce K/D region disparate graft rejection. The results thus demonstrate that a class II alloantigen on a thyroid graft may augment the rejection response directed against the graft class I alloantigens. The class II alloantigen stimulation was not always essential or sufficient for induction of class I antigen disparate thyroid graft rejection, and was dependent on the specific I region and/or K/D region gene allele.
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Mizuochi, T., S. Ono, T. R. Malek, and A. Singer. "Characterization of two distinct primary T cell populations that secrete interleukin 2 upon recognition of class I or class II major histocompatibility antigens." Journal of Experimental Medicine 163, no. 3 (1986): 603–19. http://dx.doi.org/10.1084/jem.163.3.603.
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This study has characterized the primary T cell subpopulations that secrete IL-2 in response to recognition of either class I or class II MHC encoded determinants. The addition to culture of anti-IL-2-R mAb inhibited the consumption of IL-2 by activated lymphocytes during the response period, permitting a much more accurate assessment of the amount of IL-2 produced in the response cultures. Using this response system, we found that primary T cell populations contain two IL-2-secreting T cell subsets that express reciprocal phenotypes and different MHC recognition specificities: an L3T4+, Lyt-2- T cell subset responsive to both class I and class II MHC alloantigens, and an L3T4-Lyt-2+ T cell subset responsive only to class I MHC alloantigens. The L3T4+ T cell subset expressed a broad functional response repertoire in that L3T4+ T cells were triggered to secrete IL-2 upon recognition of unmodified self-Ia determinants, allogeneic Ia determinants, and class I alloantigens presented by self-Ia determinants. The activation of L3T4+ IL-2-secreting T cells, even those responsive to class I MHC alloantigens, could be blocked completely by anti-Ia mAbs, confirming that the L3T4+ T cell subset was in fact class II restricted. In contrast, the Lvt-2+ T cell subset expressed a narrow functional response repertoire in that they were triggered to secrete IL-2 only in response to allogeneic class I MHC determinants, and were not triggered to secrete IL-2 even in response to TNP-modified self-MHC determinants. The specificity of Lyt-2+ IL-2-secreting T cells for class I MHC allodeterminants was confirmed by the observations that: (a) their activation could be blocked completely by anti-class I mAbs, (b) they could be triggered by Ia- cell lines which expressed class I MHC alloantigens and possessed accessory function, and (c) they responded to class I MHC alloantigens but failed to respond to class II MHC alloantigens, even in the presence of exogenously added second signals that circumvented the requirement for alloantigen-bearing accessory cells. Finally, the frequency of primary Lyt-2+ T cells that secreted IL-2 in response to class I (Kbm1) MHC alloantigens was shown to be only minimally lower than that of L3T4+ T cells that secreted IL-2 in response to class II (I-Abm12) MHC alloantigens.(ABSTRACT TRUNCATED AT 400 WORDS)
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Chen, Benny J., Xiuyu Cui, and Nelson J. Chao. "Human Memory T Cells Proliferate but Do Not Elicit Cytotoxicity in Response to Alloantigens." Blood 104, no. 11 (2004): 1229. http://dx.doi.org/10.1182/blood.v104.11.1229.1229.
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Abstract We and others have recently demonstrated that memory T cells do not induce graft-versus-host disease in several different animal models. To test whether the same concept applies to humans, we compared the ability of memory T cells to respond to alloantigens with that of naive as well as bulk T cells. Purified T cells were first obtained from peripheral blood from healthy donors and then separated into memory and naive T cell subsets based on the expression of CD45RA (memory: CD45RA−, naive: CD45RA+). Memory T cells were subsequently tested for their ability to respond to alloantigens using proliferation and cytotoxicity assays in comparison with naive and bulk T cells. Proliferation assay was performed using 1.25x105 responder cells and 5x105 irradiated stimulator cells per well in 96-well flat-bottom plate. Cytotoxicity was measured by the standard 4-hour Cr-51 release assay after 5-day mixed lymphocyte culture. In contrast to the mouse data, memory T cells proliferated equally well as naive and bulk T cells did in mixed lymphocyte culture (Figure A). However, these same memory T cells failed to kill the allogeneic targets despite the vigorous proliferative responses against the same alloantigens (Figure B). These data demonstrated that human memory T cells proliferate but do not elicit cytotoxicity in response to alloantigens, suggesting that human memory T cells may not contain true alloantigen-specific T cells if they have never exposed to those alloantigens before and may not cause graft-versus-host disease upon in vivo transfer. These observations warrant the further testing of human memory T cells in clinically more relevant models and in vivo for their ability to induce graft-versus-host disease. Figure Figure
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Stroncek, David. "Neutrophil alloantigens." Transfusion Medicine Reviews 16, no. 1 (2002): 67–75. http://dx.doi.org/10.1053/tmrv.2002.29406.
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Zhang, Lanfang, and Chang-Qing Xia. "PD-1/PD-L1 Interaction Maintains Allogeneic Immune Tolerance Induced by Administration of Ultraviolet B-Irradiated Immature Dendritic Cells." Journal of Immunology Research 2016 (2016): 1–11. http://dx.doi.org/10.1155/2016/2419621.
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Our previous study demonstrated that transfusion of ultraviolet B-irradiated immature dendritic cells (UVB-iDCs) induced alloantigen-specific tolerance between two different strains of mice. Programmed death-1 (PD-1) and programmed death ligand-1 (PD-L1) have been suggested to play an important role in maintaining immune tolerance. In the present study, we seek to address whether PD-1/PD-L1 plays a role in the maintenance of UVB-iDC-induced tolerance. We first observe that the UVB-iDC-induced alloantigen-specific tolerance can be maintained for over 6 weeks. Supporting this, at 6 weeks after tolerance induction completion, alloantigen-specific tolerance is still able to be transferred to syngeneic naïve mice through adoptive transfer of CD4+ T cells. Furthermore, skin transplantation study shows that the survival of allogeneic grafts is prolonged in those tolerant recipients. Further studies show that PD-1/PD-L1 interaction is essential for maintaining the induced tolerance as blockade of PD-1/PD-L1 by anti-PD-L1 antibodies largely breaks the tolerance at both cellular and humoral immunological levels. Importantly, we show that PD-1/PD-L1 interaction in tolerant mice is also essential for controlling alloantigen-responding T cells, which have never experienced alloantigens. The above findings suggest that PD-1/PD-L1 plays a crucial role in maintaining immune tolerance induced by UVB-iDCs, as well as in actively controlling effector T cells specific to alloantigens.
Dissertations / Theses on the topic "Alloantigens"
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Baker, Richard James. "Human immune responses to alloantigens." Thesis, Imperial College London, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.248200.
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Benham, Adam Maurice. "Indirect T cell allorecognition of donor MHC class I alloantigens." Thesis, University College London (University of London), 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.261866.
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Figueira, Eduardo Aleixo. "Avaliação clínica, histológica e imunológica de enxertos ósseos alógenos fresco-congelados utilizados como técnica na preservação de rebordo alveolar pós-extração." Universidade de São Paulo, 2011. http://www.teses.usp.br/teses/disponiveis/25/25146/tde-13122011-103726/.
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O osso alógeno fresco-congelado (FFBA, do inglês fresh-frozen bone allograft) é uma alternativa para os procedimentos cirúrgicos de enxerto ósseo, principalmente na preparação do rebordo alveolar para a instalação de implantes osseointegráveis. No entanto, existem alguns paradigmas que envolvem a relação entre resposta do sistema imunológico à aloantígenos presentes no enxerto e o seu comportamento clínico. Procurando entender essa relação, o FFBA foi avaliado como enxerto para preservar o rebordo alveolar pós-extração. Os resultados mostraram que embora tenha ocorrido uma redução estatisticamente significante na altura, espessura e volume do rebordo entre a avaliação inicial e final, essa redução não foi clinicamente significante, permitindo a instalação de implantes osseointegráveis. Em adição, as análises histológicas sugerem um bom comportamento do enxerto, com ausência de reação do tipo corpo estranho e formação de novo osso em todos os sítios analisados. Ao analisar o comportamento da resposta imune, os resultados mostraram que a injeção intradérmica de aloantígenos presentes no FFBA, não induziu uma reação de hipersensibilidade tardia nos pacientes após 4 meses do enxerto. Além disso, os monócitos do sangue periférico (PBMCs) dos pacientes não proliferaram frente aos aloantígenos in vitro. No entanto, os dados também demonstraram que os aloantígenos aumentam a produção de IL-2 e IFN-, mas não alteram a produção de IL-4 e IL-10, por PBMCs dos pacientes. Ao avaliar a relação entre a produção dessas citocinas e o comportamento clínico do enxerto, os dados mostram que existe uma correlação estatisticamente significante entre a produção de IL-2 in vitro e a redução (em %) da altura do rebordo alveolar, embora essa redução não tenha sido clinicamente significante. De fato, a presença de aloantígenos no FFBA não é suficiente para sua contraindicação como material de enxertia.<br>The fresh-frozen bone allograft (FFBA) is an alternative to surgical procedures of bone grafts, mainly in the preservation of alveolar ridge prior the installation of osseointegrated implants. However there are paradigms that surround the relation between immune response to alloantigens present inside the graft and the clinical response of the graft. An attempt to understand this relationship, the FFBA was evaluated as a graft to preserve the alveolar ridge post-extraction. The results show a statistically significant reduction in height, thickness and volume of the ridge between the initial and final examination, however this reduction was not clinically significant. The ridge preservation allowed implant installation and osseointegration. In addition, histologic analysis suggests a good performance of the graft with no foreign body reaction and formation of new bone at all sites. In analyzing the behavior immune response, the results showed that stimulation with alloantigens present in bone allograft induced no delayed hypersensitivity reaction in vivo. Additionally, periphery blood mononuclear cells (PBMC) from patients no proliferate in response to alloantigens in vitro. However, the data also demonstrated that the alloantigens increase IL-2 and IFN- production, but no IL-4 and IL-10 production, by PBMCs from patients. When evaluate the relation between the cytokines production and clinical parameters, the results demonstrate that there statistically significant correlation between IL-2 production in vitro and ridge height changes (%), although this clinical parameter is not clinically significant. In fact, the alloantigens in FFBA are not sufficient for its contraindications as grafting material.
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Goodacre, J. A. "A study of the frequency of mouse cells which present alloantigens and ovalbumin to T lymphocytes." Thesis, University of Newcastle Upon Tyne, 1988. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.233305.
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Leber, Anne. "Untersuchungen zur Generierung, Migration und Funktion von Regulatorischen T-Zellen in der Schwangerschaft." Doctoral thesis, Humboldt-Universität zu Berlin, Mathematisch-Naturwissenschaftliche Fakultät I, 2011. http://dx.doi.org/10.18452/16394.
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Ein wichtiges Merkmal der normalen Schwangerschaft ist die Toleranz des mütterlichen Immunsystems gegenüber den fremden fetalen Antigenen. Regulatorische T-Zellen (Treg-Zellen) steigen während der frühen Schwangerschaft an und leisten einen entscheidenden Beitrag zur fetalen Toleranz. Allerdings sind die genauen Mechanismen ihres Anstieges und ihrer Wirkungsweise noch weitgehend ungeklärt. Erste Untersuchungen zeigten, dass die Anzahl an Treg-Zellen in der empfänglichen Phase des Estruszyklus in der Maus am höchsten war. Es kann vermutet werden, dass die erhöhte Anzahl an Treg-Zellen zum Zeitpunkt der Insemination eine frühe Erkennung von väterlichen Antigenen begünstigt und somit zur Vorbereitung des mütterlichen Immunsystems auf die Implantation des Embryos beiträgt. Weiterhin konnte nachgewiesen werden, dass Alloantigene im Ejakulat den frühen Anstieg der Treg-Zellen in der Schwangerschaft bedingen und dass das in der Samenblasenflüssigkeit enthaltene Zytokin TGF-beta die Expansion der Treg-Zellen unterstützt. Diese Ergebnisse befürworten eine Alloantigen-vermittelte Expansion der Treg-Zellen während der frühen Schwangerschaft, die darüber hinaus durch TGF-beta begünstigt wird. Im Rahmen dieser Arbeit konnte ebenfalls belegt werden, dass das Schwangerschaftshormon hCG einen entscheidenden Einfluss auf die Treg-Zellen im Verlauf der Schwangerschaft ausübt. Untersuchungen unter Verwendung von menschlichem Probenmaterial konnten deutlich zeigen, dass hCG die Migration von Treg-Zellen zu Trophoblasten vermittelt und zur Konvertierung von konventionellen T-Zellen in Treg-Zellen beiträgt. Darüber hinaus konnten Versuche im Mausabortmodell zeigen, dass die Applikation von hCG die Expansion und Funktion der Treg-Zellen entscheidend beeinflusst, wodurch das Auftreten von Aborten in Abortweibchen verhindert werden konnte. HCG vermittelt demnach die Generierung, Migration und Funktion der Treg-Zellen und trägt entscheidend zum erfolgreichen Verlauf der Schwangerschaft bei.<br>Normal pregnancy is characterized by the generation of maternal immune tolerance towards the foreign fetal antigens. Regulatory T cells (Treg cells) have been shown to increase in number during early pregnancy stages and to be essential for the establishment of fetal tolerance. However, the mechanisms and factors supporting their increase and function are not well defined. First investigations showed that Treg cells accumulated in the sexually receptive phase of the murine estrous cycle. Thus, it can be assumed that the accumulation of Treg cells around the time of insemination favours early recognition of paternal antigens and thereby prepares the maternal immune system for the implantation of the blastocyst into the maternal endometrium. Experiments investigating the increase of Treg cells during early pregnancy suggest that alloantigens present in the ejaculate mediated early Treg cell augmentation. Moreover TGF-beta, which represents a major component in the seminal fluid, provoked the proliferation of Treg cells. These results suggest that the early expansion of Treg cells is alloantigen-mediated and that seminal fluid-derived TGF-beta is involved in this expansion. Additionally it has been shown that the pregnancy hormone human Chorionic Gonadotropin (hCG) has an important impact on Treg cells during pregnancy. By using human samples it has been proven that hCG mediates the migration of Treg cells to trophoblast cells and supports the conversion of naïve T cells into Treg cells directly at the fetal-maternal interface. In mice, the application of hCG resulted in an increase in the number and function of Treg cells and thereby prevented abortion in a mouse abortion-prone model. Thus, hCG mediates the generation, migration and function of Treg cells and contributes to a successful pregnancy outcome.
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Opiela, Shannon Jacqueline. "Neonatal T Cell Responses are Highly Plastic: I. Neonates Generate Robust T Cell Responses against Alloantigens II. Functional Capabilities of Neonatal RTE are more Diverse than Adult RTE." Scholarly Repository, 2008. http://scholarlyrepository.miami.edu/oa_dissertations/139.
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Neonatal immune responses are typically deficient against a wide variety of antigens, including alloantigens, vaccine antigens, and infectious agents. These responses are characterized by Th2-skewed cytokine production, and deficient Th1 and cytotoxic responses. However, these deficient responses can be boosted to adult levels by the use of strong, Th1 promoting agents. This demonstrates that neonates are capable of developing mature immune responses under specific conditions. Using two different murine models, we have found that neonates develop robust Th and cytotoxic responses, which under some antigenic conditions significantly exceed those of adults. First, using a model of early life exposure to noninherited maternal antigens (NIMA), we found that murine neonates develop robust in vivo cytotoxic responses to low doses of alloantigens. Importantly, primary in vivo cytotoxic responses to alloantigen developed during the neonatal period, and persisted into adulthood. Neonates developed similar memory cytotoxic responses to donor spleen cells, bone marrow, and stem cell-enriched (Lin-) bone marrow cells, suggesting that the exposure dose is more important than the type of transplanted donor cell for the development of cytotoxicity. NIMA-exposed neonates also developed vigorous primary and memory allospecific Th1/Th2 responses which exceeded the responses of adults. These findings suggest that early exposure to low levels of NIMA may lead to long term immunological priming of all arms of T cell adaptive immunity. Second, we characterized the phenotype and function of neonatal recent thymic emigrants (RTE). RTE are the predominant cell type in murine neonates, and are present at higher frequencies within the neonatal CD4+ compartment than in adults. Our data demonstrate that RTE from murine neonates and adults are phenotypically and functionally distinct. In particular, although the magnitude of RTE cytokine responses from both age groups is dependent on the conditions of activation, neonatal RTE consistently exhibited higher levels of effector cytokine production than adult RTE. In particular, activation of neonatal RTE in the presence of IL-7 lead to greatly increased IFNgamma production, while adult responses were not altered. Overall, neonatal RTE responses were more plastic than those of adult RTE, as both Th1 and Th2 responses were altered in neonates using various activation conditions, while only Th2 responses were consistently changed in adults. Finally, in contrast to adult RTE, neonatal RTE proliferated in response to IL-7 stimulation at very early timepoints. This was associated with faster kinetics of IL-7Ralpha downregulation and higher levels of pSTAT5 in neonatal RTE. These quantitative and qualitative differences in neonatal RTE populations may largely explain the diverse responses that are elicited in neonates in response to different antigens, especially under those conditions in which Th1 responses are enhanced (i.e., exposure to NIMA alloantigens). Taken together, these data demonstrate that neonatal T cell responses are actually highly plastic, instead of intrinsically deficient. Furthermore, if given optimal stimulation conditions, neonatal responses can actually exceed those produced by adults.
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Pereira, Fabiana de Souza. "Frequência dos antigenos e anticorpos neutrofílicos humanos (HNA) em doadores e receptores de transplante alogênico de célula tronco hematopoiética (TCTH) e sua correlação com doença enxerto contra hospedeiro (DECH) aguda." reponame:Biblioteca Digital de Teses e Dissertações da UFRGS, 2015. http://hdl.handle.net/10183/139761.
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Background e objetivo. A reconstituição celular hematopoiética com o transplante de células tronco hematopoiéticas (TCTH) alogênicas é um método de tratamento estabelecido para uma variedade de doenças hematológicas, oncológicas e imunológicas. Entretanto, TCTH está associado a considerável morbimortalidade devido a fatores como recidiva da doença de base, grau de compatibilidade HLA, tipo de regime de condicionamento e infecções durante o período de neutropenia. Este estudo investigou a associação entre o aloantígenoneutrofílico humano (HNA) e o dia de pega, a ocorrência de DECH aguda e TRM em pacientes que foram submetidos a transplante de células tronco hematopoiéticas alogênico. Tipo de estudo e local. Estudo de coorte prospectivo realizado no Hospital de Clínicas de Porto Alegre. Métodos. Avaliamos 27 pacientes transplantados entre maio de 2013 e abril de 2014 e seus respectivos doadores. A tipagem HNA foi realizada, nas amostras dos doadores, por PCR-SSP e os anticorpos anti-HNA foram detectados nos pacientes utilizando o kit LABSCREEN MULTI (LSMUTR – One Lambda). Resultados. A idade variou entre 1 a 63 anos, com uma média de 20,4 ± 17,5 anos. Dezenove pacientes eram pediátricos (<21 anos) com média de idade de 10,05 ± 6,4 anos e entre os pacientes adultos a média foi 42,2 ± 12,6 anos. Houve um discreto predomínio do sexo masculino 16 (59,3%). As leucemias agudas foram frequentes em 19 (70,4%) dos pacientes, outras doenças oncohematológicas malignas (Linfoma Hodgkin e Linfoma não Hodgkin) estiveram em 3 (11,1%) e as não malignas (síndrome mielodisplásica, osteopetrose, hemoglobinúria paroxicística noturna, aplasia e doença granulomatosa) estiveram em 6 (22,2%) dos casos. A maioria dos pacientes 19 (70,4%), apresentavam a doença há menos de 12 meses na época do transplante e 24 (88,9%) deles foram totalmente compatível com seus doadores quanto ao sistema HLA. O regime de condicionamento mieloablativo foi utilizado em 16 (59,2%) dos pacientes e a profilaxia padrão para DECH (ciclosporina e metotrexate) foi utilizada em 15 (55,5%) dos pacientes. O dia de pega teve uma mediana de 19 e mínimo e máximo de 15 e 30, respectivamente. Quatro pacientes (14,8%) tiveram óbito antes da pega. Aproximadamente 63% (17 pacientes) apresentaram DECH aguda (em todos os estágios) e a taxa de mortalidade (TRM) foi de aproximadamente 44% dos casos (12 pacientes). Os pacientes que receberam TCTH de um doador aparentado tiveram TRM de aproximadamente 41% (7 pacientes) e os que receberam de um doador não aparentado foi de aproximadamente 45% (5 pacientes). A frequência dos antígenos HNA detectados nos doadores foi de 46,4% HNA-1a, 89,3% HNA-1b, 3,6% HNA-1c, 96,4% HNA-3a, 32,1% HNA-3b, 96,4% HNA-4a, 21,4% HNA-4b, 85,7% HNA-5a e 71,4% HNA-5b. A frequência dos anticorpos anti-HNA1a, anti-HNA1b, anti-HNA1c e anti-HNA2 no D0 foram respectivamente 46,4%, 42,9%, 42,9% e 53,6%. A associação entre a tipagem HNA dos doadores e anticorpos anti-HNAdos receptores com dia da pega, DECH aguda e TRM não mostrou correlação estatisticamente significativa. Conclusão. A frequência de HNA encontradanos doadores está de acordo com o descrito pela literatura. Contudo, a frequência dos anticorpos anti-HNAs foi bastante alta na população do estudo, embora a maioria apresentasse doença há menos de 12 meses até o transplante. Apesar de não encontrarmos uma correlação, novos estudos são necessários para melhor avaliar o papel do HNA no desfecho do TCTH.<br>Background and purpose. Hematopoietic cellular reconstruction with allogeneic hematopoietic stem cell transplantation (HSCT) is an established method of treatment for a variety of hematological, oncologic and immunologic diseases. However, HSCT is associated with considerable morbidity and mortality due to recurrence of underlying disease, incomplete HLA compatibility, type of conditioning regimen and infection during the unavoidable period of neutropenia. This study investigates a surrogate cause of morbidity: compatibility of Human Neutrophil Antigens (HNA) between donors and receivers and its association with day of engraftment, incidence of acute graft versus host disease (GVHD) and total rate of mortality (TRM) in patients who underwent allogeneic HSCT. Type of study and location. Prospective cohort study carried out at the Hospital de Clínicas de Porto Alegre (HCPA), Brazil. Methods. We have studied 27 patients who underwent HSCT between May, 2013 and April, 2014, and their respective donors. HNA typing in the donors was performed by PCR-SSP (One Lambda) and anti-HNA antibodies in receivers were detected using the LABSCREEN MULTI kit (LSMUTR-One Lambda). Results. The age ranged from 1 to 63 years, with an average of 20.4 ± 17.5 years. Nineteen were pediatric patients (<21 years) with an average age of 10.05 ± 6.4 years, and among adult patients the average was 42.2 ± 12.6 years. There was a discreet male prevalence, 16 (59,3%). The acute leukemias were frequent in 19 (70,3%) of patients, other malignant onco-hematological diseases (Hodgkin Lymphoma and non-Hodgkin's Lymphoma) in 3 (11,1%) and non-malignant (myelodysplastic syndrome, osteopetrosis, paroxysmal nocturnal hemoglobinuria, aplasia and granulomatous disease) in 6 (22,2%). Nineteen (70,3%) of the patients, had the disease for less than 12 months at the time of the transplant and 24 (88,9%) were fully HLA compatible with their donors. Myeloablative conditioning regimen was used in 16 (59,3%) of the patients and the standard prophylaxis for GVHD (cyclosporine and methotrexate) was used in 15 (55,5%) of the patients. The day of engraftment had a median of 19 and minimum and maximum of 15 and 30, respectively. Four patients (14,8%) died before the engraftment. Approximately 17 patients (63%) showed acute GVHD (in all stages) and the total rate of mortality (TRM) was approximately 44% of the cases (12 patients). Patients who received HSCT from a related donor had TRM of approximately 41% (7 patients) and those who have received an unrelated donor was approximately 45% (5 patients). The frequency of HNA antigens detected in donors was 46,4% HNA-1a, 89,3% HNA-1b, 3,6% HNA-1c, 96,4% HNA-3a, 32,1% HNA-3b, 96,4% HNA-4a, 21,4% HNA-4b, 85,7% HNA-5a and 71,4% HNA-5b. The frequency of antibodies anti-HNA1a, anti-HNA1b, anti-HNA1c and anti-HNA2 at D0 were respectively 46,4%, 42,9%, 42,9% and 53,6%. The association between the HNA donor typing and anti-HNA antibodies of receivers with day of the engraftment, acute GVHD and TRM showed no statistically significant correlation. Conclusion. The HNA frequency found in our donors was close to the described in the literature. The frequency of anti-HNAs antibodies, however, was quite high in our study population; although the majority presented the disease for less than 12 months before the transplant. The association between HNA donor typing and anti-HNA antibodies of patients with day of engraftment, acute GVHD incidence and TRM showed no statistically significant correlation. As the number of cases was small, further studies with higher numbers and with antigen/antibodies assayed in both sides of transplantation pairs, are needed to better assess the role of the HNAs on the outcome of HSCT.
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Fluck, Nicholas C. "Immunological events resulting from intrathymic delivery of alloantigen." Thesis, University of Oxford, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.312492.
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Hoff, Uwe. "Bedeutung der Alloantigen-unabhängigen Faktoren in der Frühphase nach tierexperimenteller Nierentransplantation." [S.l.] : [s.n.], 2005. http://deposit.ddb.de/cgi-bin/dokserv?idn=974978132.
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Seltrecht, Nadja [Verfasser]. "Alloantigen-spezifische regulatorische T-Zellen zur Toleranzinduktion nach Organtransplantation / Nadja Seltrecht." Hannover : Technische Informationsbibliothek und Universitätsbibliothek Hannover (TIB), 2012. http://d-nb.info/1022810782/34.
Full textBook chapters on the topic "Alloantigens"
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Pai, Shun-Chung, and Liang-In Lin. "Sequence-Based Typing for Platelet alloantigens." In Molecular Typing of Blood Cell Antigens. Springer New York, 2015. http://dx.doi.org/10.1007/978-1-4939-2690-9_14.
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Crumpton, Michael J. "Alloantigens on leukocytes and platelets: Biochemistry." In Advances in Forensic Haemogenetics. Springer Berlin Heidelberg, 1988. http://dx.doi.org/10.1007/978-3-642-73330-7_9.
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Varewyck, H., and Y. Bouquet. "Ela(Equine Lymphocyte Alloantigens) Serology and Genetics." In Improving Genetic Disease Resistance in Farm Animals. Springer Netherlands, 1989. http://dx.doi.org/10.1007/978-94-009-1057-7_5.
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Gorakshakar, Ajit, and Harita Gogri. "Alloantigens and Their Role in Immune Cytopenias." In Hematopathology. Springer Singapore, 2019. http://dx.doi.org/10.1007/978-981-13-7713-6_27.
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Root-Bernstein, Robert S., and Sheila Hobbs DeWitt. "Semen alloantigens and lymphocytotoxic antibodies in AIDS and ICL." In AIDS: Virus- or Drug Induced? Springer Netherlands, 1996. http://dx.doi.org/10.1007/978-94-009-1651-7_16.
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Streilein, J. W., C. Arancibia-Caracamo, and H. Osawa. "The Role of Minor Histocompatibility Alloantigens in Penetrating Keratoplasty." In Adequate HLA Matching in Keratoplasty. KARGER, 2002. http://dx.doi.org/10.1159/000067655.
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Duijvestijn, A., L. Vlek, L. Duistermaat, H. van Rie, and P. van Breda Vriesman. "Chronic renal allograft rejection: the significance of non-MHC alloantigens." In Transplant International Official Journal of the European Society for Organ Transplantation. Springer Berlin Heidelberg, 1992. http://dx.doi.org/10.1007/978-3-642-77423-2_188.
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Dahr, W. "Alloantigens of Proteins and Glycoproteins in Membranes of Human Red Blood Cells." In Advances in Forensic Haemogenetics. Springer Berlin Heidelberg, 1988. http://dx.doi.org/10.1007/978-3-642-73330-7_2.
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Wagner, H., K. Pfeffer, and K. Heeg. "Induction of Peripheral Tolerance to Class I MHC Alloantigens in Adult Mice." In Pathways in Applied Immunology. Springer Berlin Heidelberg, 1991. http://dx.doi.org/10.1007/978-3-642-76606-0_8.
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Kleesiek, K., C. Götting, J. Diekmann, J. Dreier, and M. Schmidt. "Alloantigene." In Lexikon der Medizinischen Laboratoriumsdiagnostik. Springer Berlin Heidelberg, 2018. http://dx.doi.org/10.1007/978-3-662-49054-9_152-1.
Full textConference papers on the topic "Alloantigens"
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Kawai, Y., R. R. Montgomery, K. Furihata, and T. J. Kunicki. "EXPRESSION OF PLATELET ALLOANTIGENS ON HUMAN ENDOTHELIAL CELLS AND HEL CELLS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1642813.
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Analogs of platelet membrane glycoproteins IIb and IIIa (GPIIb-IIIa) have been shown to be synthesized and expressed by human endothelial cells (HEC), a human erythroleukemia cell line (HEL) and various other cells. Previous studies from our laboratory demonstrated that the platelet alloantigen P1A1, is expressed on HEC GPIIIa. Other alloantigen systems, namely, Pen and Bak, are known to be localized on platelet GPIIIa and GPIIb, respectively. Utilizing additional antibodies from patients with PTP specific for Pena, Baka, and Bakb allo-antigens, and isoantibodies (iso-ab) from a patient with Glanzmann's Thrombasthenia (GT), we have studied cultured HEC and HEL cells for expression of epitopes recognized by these antibodies. HEC and HEL cells were meta-bolically labeled with 35S-methionine and lysed in 0.5% TX-100 in the presence of 5mM EDTA. Soluble antigens were immunoprecipitated with these antibodies coupled to Protein A-Sepharose and subjected to SDS-PAGE and fluorography. Anti-Pena and the GT iso-ab reacted with the GPIIb-IIIa complex from both HEC and HEL lysates, but anti-Baka and anti-Bakb failed to immunoprecipitate GPIIb-IIIa analogs from either HEC or HEL. In an immunoblot assay, the GT iso-ab bound to GPIIIa of both HEC and HEL. Anti-Pena failed to react with SDS-denatured proteins. HEL GPIIIa migrates slightly faster than HEC GPIIIa and slightly slower than platelet GPIIIa. These results indicate that the epitopes of platelet GPIIIa recognized by alloantibodies and isoantibodies are shared by GPIIIa analogs of HEC and HEL. GPIIb-associated alloantigens are not expressed by HEC and HEL GPIIb analogs, an observation that is consistent with the decreased structural homology between GPIIb analogs derived from different cell types.
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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.
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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.
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Schreiber, A. B., R. Gillette, and M. E. Hrinda. "IN VITRO IMMUNE PARAMETERS OF MONOCLATEH, A, MONOCLONAL ANTIBODY PURIFIED HUMAN PLASMA FACTOR VIII:C THERAPEUTIC PREPARATION." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644051.
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MonoclateR is a highly purified human factor VIII:C preparation obtained by immunoaffinity chromatography of plasma cryoprecipitat followed by chromatography on aminohexyl sepharose. The resulting product is devoid of alloantigens, can be stabilized in the absence of extraneous human proteins and has a specific activity higher than 3000 U/mg.To ascertain product integrity, we set out to compare MonoclateR preparations with either unfractionated human plasma, cryoprecipitateor commercially available lyophilized antihemophilia factor (AHF) preparations by Western blots. As probes, we utilized a series of monoclonal antibodies to defined factor VIII:C epitopes. The MonoclateR VIII:C chain composition appeared indistinguishable from that in the native state of in commercial, clinically useful preparations.Patients with hemophilia are often afflicted with an impairment of cell-mediated immunity, when treated repeatedly with plasma cryoprecipitate preparations. Those preparations, containing at best 0.2% factor VIII:C in protein content, were found in our hands to dramatically inhibit both human mixed lymphocyte reactions and the phytohemagglutinin induced human lymphocyte mitogenesis. We obtained 50% inhibition at about 1 mg/ml protein concentration. These effects were not due to cytotoxicity nor related to procoagulant potency.MonoclateR, in contrast, was totally devoid of immunosuppressive activity at all concentrations tested. This in vitro finding may be related to clinical observation of corrections in immune impairment in adult hemophiliacs treated with MonoclateR. With this immunological profile, MonoclateR represents in our opinion, a promising novel treatment modality for hemophilia A.
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Santoso, S., Y. Shibata, V. Kiefel, and C. Mueller-Eckhardt. "IDENTIFICATION OF YUK(b) ALLOANTIGEN ON PLATELET GLYCOPROTEIN IIIa*." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643528.
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Neonatal alloimmune thrombocytopenic purpura (NATP) is caused by IgG platelet alloantibodies (ab), produced by the mother and directed against antigens present on the platelets of the child. The specificity of the platelet-specific ab is anti-Pl(Al) in the majority of cases. Other specificities, i.e. anti-Pl(E2), anti-Bak(a), anti-Pen, and anti-Pl(A2) have also been found. Recently, Shibata et al (1986) have described a new platelet antigen system Yuk(a)/Yuk(b) involved in NATP. The Yuk(a) and Yuk(b) antigens are not expressed on thromb-asthenic platelets indicating that these antigens do exiŞt on glycoprotein (GP) lib and/or Ilia. In order to investigate the molecular localization of these antigens, we studied the interaction of anti-Yuk(b) purified ab with membrane components of platelets using immunoblot procedure and compared their immunochemical behaviour with that of other platelet specific ab (anti-Pl(A 1), -Lek(a), -Bak(a)).In the absence of disulfide reduction Yuk(b) ab reacted with an antigen of molecular weight (mol wt) 92 kDa with an electrophoretic mobility identical to GP Ilia. An identical result was obtained for P1(A1) ab. In contrast, the Bak(a) ab as well as Lek(a) ab detected an antigen of mol wt 134 kDa which comigrated with GP lib. After reduction with 2-mercaptoethanol binding of anti-Pi(Al) and anti-Yuk(b) was not observed. To further localize the Yuk(b) antigen on GP Ilia, immunoblotting experiments were performed with anti-Pl(Al) and anti-Yuk(b) of chymotrypsin treated platelets. While anti-Pl(Al) bound to GP IIIa and a 68 kDa component, anti-Yuk(b) bound only to GP IIIa when the platelets had been treated for 45 min with chymotrypsin.This discrepancy became even more pronounced by prolonged treatment of platelets (225 min) in that the reactivity of anti-Yuk(b) was entirely abolished, whereas binding of anti-Pl(Al) shifted completely from the 92 kDa to the 68 kDa component. Thus, unlike the P1(A1) antigen, the Yuk(b) determinant either resides on the 30 kDa fragment of GP Ilia or it is destroyed by chymotrypsin treatment.
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Giltay, J. C., O. C. Leeksma, A. E. G. Kr v. d. Borne, and J. A. van Mourik. "THE PLATELET ALLOANTIGEN Zwa (P1A1) IS EXPRESSED BY CULTURED ENDOTHELIAL CELLS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1642812.
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Zwa (P1A1) is a platelet specific alloantigen, located on glycoprotein (GP) IIIa, and is of pathogenic importance in alloimmunologic disorders such as neonatal alloimmune thrombocytopenia and post transfusion purpura. As endothelial cells synthesize a plasma membrane protein complex which is structurally closely related to the platelet membrane GP IIb/IIIa complex, we examined whether these cells also express Zwa. Employing a variety of immunochemical techniques, our studies show that endothelial cells indeed can express this antigen at the plasma membrane surface.We also compared the expression of Zwa on platelets, isolated from umbilical cord blood, with the expression of Zwa on cultured endothelial cells, isolated from the same umbilical cord, of a number of neonates. Both platelets and endothelial cells obtained from the same individual, either expressed Zwa (Zwa positive individuals) or lacked expression of Zwa (Zwa negative individuals). These findings strongly suggest that endothelial-and platelet Zwa are encoded by the same genes.Thus, Zwa is not exclusively expressed by platelets, also endothelial cells express this alloantigen.An important consequence could be, that in alloimmunologic disorders in which the Zwa antigen is implicated, not only the platelets, but also the vessel wall is involved.
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Mercadante, Ana Carolina T., Suelen Perobelli, Ana Paula G. Alves, et al. "Abstract 2590: Oral combined therapy with probiotics and alloantigen induces B cell dependent long lasting specific tolerance." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-2590.
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Giltay, J. C., O. C. Leeksma, C. Breederveld, and J. A. van Mourik. "NORMAL SYNTHESIS AND EXPRESSION OF ENDOTHELIAL GP IIb/IIIa IN GLANZMANN'S THROMBASTENIA." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1642817.
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In Glanzmann’s thrombastenia (GT), an autosomal recessive inherited hemorrhagic disease, the platelet membrane glycoprotein (GP) IIb/IIIa complex is absent or reduced. Recently we and others demonstrated that cultured human umbilical vein endothelial cells synthesize a membrane protein complex that is structurally closely related to GP IIb/IIIa. Endothelial cells of thrombasthénie patients could, therefore be deficient in GP IIb/IIIa. We had the opportunity to culture endothelial cells isolated from the umbilical cord of a newborn with GT and to examine the plasma membrane composition of these cells. Employing a variety of immunochemical techniques, including immunoprecipitation, immunofluorescence staining and crossed immunoelectrophoresis, we demonstrated that the endothelial cells of the patient were indistinguishable from normal endothelial cells in their ability to synthesize and express GP IIb/IIIa. Our results indicate that GT is not accompanied by and "endotheliopathy".Zwa (P1A1) is an alloantigen, located on platelet GP IIIa, and, consequently, Zwa is absent on GT platelet. Data will he presented which show that not only normal endothelial IIIa carries the Zwa antigen, hut also GT endothelial cells normally express Zwa. This finding supports our view that GT endothelial GP IIb/IIIa is indistinguishable from normal endothelial GP IIb/IIIa. Moreover, this finding directly shows that the thrombastenic glycoprotein abnormality and the inheritance of Zwa antigen are controlled by different genes.
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Vokac, KA, J. Ferrars, and RR Montgomery. "RISTOCETIN-INDUCED ENDOTHELIAL CELL BINDING OF PLASMA VON WILLEBRAND FACTOR." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1642913.
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Our laboratory previously used a technique of labeling plasma von Willebrand factor (vWf) with radiolabeled AVW1 - a “ neutral” monoclonal antibody to vWf. This technique has been used to study the binding of plasma vWf to platelets in the plasma milieu. Studies by several laboratories including ours have demonstrated structural glycoproteins on endothelial cells that are analogous to platelet GP Ilb/IIIa and we have shown that the platelet alloantigen Pl-Al is expressed on the surface of cultured endothelial cells. We undertook this study to evaluate the binding of plasma vWf to cultured endothelial cells in confluent monolayer cultures using the “ neutral” monoclonal antibody technique. Plasma vWf was “ labeled” using trace quantities of radiolabeled AVW-1. We then added 80,000 cpm of monoclonal-labeled plasma to 48 well culture plates containing confluent secondary cultures of human umbilical vein endothelial cells. Following the addition of ristocetin, the plates were incubated for 1 hour at room temperature, centrifuged, and the count8 bound and the counts remaining in the supernate were determined. In the presence of ristocetin, 67.5% of the labeled vWf bound to the endothelial cells. When “ labeled“ severe von Willebrand plasma was used or when ristocetin was omitted, less than 5% of the counts bound. Controls using mouse serum or excess mouse IgG to rule out Fc receptor binding and controls to evaluate binding to the subcellular matrix were performed and demonstrated this binding to be vWf and cell surface dependent. Unlike platelet vWf binding, this binding was not inhibited by monoclonal or polyclonal antibodies to platelet GPIb. We studied plasma from patients with type I, a variant of type I, and type Ila vWd and found normal binding with the type I plasma, but reduced binding with the type I variant plasma (14.5%) and the type Ila plasma (7.1%). AVW3, a monoclonal antibody to vWf that blocks vWf binding to platelet GPIb, blocked vWf binding to endothelial cells. Endothelial cells, like platelets, have the ability to bind plasma von Willebrand factor in the presence of ristocetin. This phenomenon occurs on the surface of endothelial cells in culture. Qualitative and quantitative reductions of this vWf binding are found with the plasma of patients with von Willebrand’s disease.