Добірка наукової літератури з теми "Activation polyclonal"
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Статті в журналах з теми "Activation polyclonal":
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Goldman, Michel, Dana Baran, and Philippe Druet. "Polyclonal activation and experimental nephropathies." Kidney International 34, no. 2 (August 1988): 141–50. http://dx.doi.org/10.1038/ki.1988.159.
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Chequer-Bou-Habib, Dumith, Claudio Daniel-Ribeiro, Dalma M. Banic, Antonio C. Franciscone do Valle, and Bernardo Galvao-Castro. "Polyclonal B cell activation in paracoccidioidomycosis." Mycopathologia 108, no. 2 (November 1989): 89–93. http://dx.doi.org/10.1007/bf00436058.
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Dziarski, Roman. "Autoimmunity: polyclonal activation or antigen induction?" Immunology Today 9, no. 11 (January 1988): 340–42. http://dx.doi.org/10.1016/0167-5699(88)91333-3.
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Tew, John, David Engel, and Dennis Mangan. "Polyclonal B-cell activation in periodontitis*." Journal of Periodontal Research 24, no. 4 (July 1989): 225–41. http://dx.doi.org/10.1111/j.1600-0765.1989.tb01787.x.
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Kaattari, Stephen L., and Mary A. Yui. "Polyclonal activation of salmonid B lymphocytes." Developmental & Comparative Immunology 11, no. 1 (December 1987): 155–65. http://dx.doi.org/10.1016/0145-305x(87)90017-6.
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Barbieri, P., I. Olivieri, G. Benedettini, P. Marelli, M. L. Ciompi, G. Pasero, and M. Campa. "Polyclonal B cell activation in ankylosing spondylitis." Annals of the Rheumatic Diseases 49, no. 6 (June 1, 1990): 396–99. http://dx.doi.org/10.1136/ard.49.6.396.
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Granholm, Norman A., and Tito Cavallo. "Autoimmunity, Polyclonal B-Cell Activation and Infection." Lupus 1, no. 2 (February 1992): 63–74. http://dx.doi.org/10.1177/096120339200100203.
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Burg, Debra L., and Thomas L. Feldbush. "Polyclonal activation of primed rat B cells." Cellular Immunology 98, no. 2 (April 1986): 351–63. http://dx.doi.org/10.1016/0008-8749(86)90295-9.
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Neveu, P. J., and D. Perdoux. "Polyclonal Activation of Guinea Pig Spleen Lymphocytes." International Archives of Allergy and Immunology 78, no. 4 (1985): 401–5. http://dx.doi.org/10.1159/000233921.
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Donati, Daria, Li Ping Zhang, Qijun Chen, Arnaud Chêne, Kirsten Flick, Maja Nyström, Mats Wahlgren, and Maria Teresa Bejarano. "Identification of a Polyclonal B-Cell Activator in Plasmodium falciparum." Infection and Immunity 72, no. 9 (September 2004): 5412–18. http://dx.doi.org/10.1128/iai.72.9.5412-5418.2004.
Анотація:
ABSTRACT Polyclonal B-cell activation and hypergammaglobulinemia are prominent features of human malaria. We report here that Plasmodium falciparum-infected erythrocytes directly adhere to and activate peripheral blood B cells from nonimmune donors. The infected erythrocytes employ the cysteine-rich interdomain region 1α (CIDR1α) of P. falciparum erythrocyte membrane protein 1 (PfEMP1) to interact with the B cells. Stimulation with recombinant CIDR1α induces proliferation, an increase in B-cell size, expression of activation molecules, and secretion of immunoglobulins (immunoglobulin M) and cytokines (tumor necrosis factor alpha and interleukin-6). Furthermore, CIDR1α binds to Fab and Fc fragments of human immunoglobulins and to immunoglobulins purified from the sera of different animal species. This binding pattern is similar to that of the polyclonal B-cell activator Staphylococcus aureus protein A. Our findings shed light on the understanding of the molecular basis of polyclonal B-cell activation during malaria infections. The results suggest that the var gene family encoding PfEMP1 has evolved not only to mediate the sequestration of infected erythrocytes but also to manipulate the immune system to enhance the survival of the parasite.
Дисертації з теми "Activation polyclonal":
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Haidar, ahmad Hamad. "Pro-inflammatory activity and adjuvant effect of Neutrophil Extracellular Traps in physiological and pathological context." Electronic Thesis or Diss., Paris 13, 2024. http://www.theses.fr/2024PA131004.
Анотація:
Les neutrophiles activés (PNNs) expulsent des "Neutrophil extracellular traps" (NETs). Les NETs constituent un mécanisme de défense contre les agents pathogènes. Cependant, le rôle des NETs va au-delà de leur fonction antimicrobienne, avec des implications dans divers processus physiologiques et pathologiques, y compris les troubles auto-immuns. Une augmentation de la formation des NETs a été signalée dans la polyarthrite rhumatoïde (PR); une maladie inflammatoire chronique touchant les articulations. Nous avons précédemment montré que les NETs sont pro-inflammatoires sur les macrophages au repos. En effet, les NETs contiennent plusieurs molécules ayant des propriétés immunostumulatrices. Nous suggérons que les NETs agissent comme des motifs moléculaires associés aux dommages (DAMPs) sur les lymphocytes B en induisant leur activation polyclonale, indépendamment de la spécificité de l'antigène ; un nouveau mécanisme par lequel les NETs pourraient contribuer à la dérégulation immunitaire, en particulier dans le contexte de la PR. Nous avons démontré par cytométrie de flux, ELISA et séquençage des ARN (RNAseq) que les NETs pouvaient directement activer les cellules B totaux et naïves vers un profil pro-inflammatoire robuste, caractérisé par une production élevée de cytokines pro-inflammatoires et une surexpression de HLA-DR et des molécules de co-stimulation CD40 et CD86 qui sont importantes pour la fonction de cellules présentatrices d'antigènes (CPA). Cette activation est amplifiée chez les patients atteints de PR. Nous avons également montré que ce mécanisme est modulé par la présence des protéines C1q et de LL-37 mais qu'il ne nécessite pas le "Toll-like receptor 9" (TLR9). Au-delà de l'activation des cellules B, nos résultats mettent en lumière l'effet domino initié par les NETs. Les cellules B activées par les NETs agissent ensuite comme CPA et déclenchent l'activation des cellules T, renforçant ainsi la réponse immunitaire adaptative. Les cellules B activées par les NETs induisant également le recrutement et l'activation des neutrophiles. Cette interaction potentielle met en évidence la nature polyvalente des NETs au-delà de leur rôle conventionnel dans la défense antimicrobienneActivated neutrophils (PMNs) expel neutrophil extracellular traps (NETs). NETs serve as adefense mechanism against pathogens. However, the role of NETs extends beyond their antimicrobial function, with implications in various physiological and pathological processes, including autoimmune disorders. Increased NET formation has been reported in rheumatoid arthritis (RA); a chronic inflammatory disease affecting joints. We have previously shown that NETs are pro-inflammatory on resting macrophages. Indeed, NETs contain several molecules with immunostumulatory properties. We suggest that NETs act as damage-associated molecular patterns (DAMPs) on B lymphocytes inducing their polyclonal activation, independently of antigen specificity; a new mechanism by which NETs might contribute to immune dysregulation, particularly in the context of RA. We demonstrate by flow cytometry, ELISA and RNA sequencing (RNAseq) that NETs could directlyactivate total and naïve B cells toward a robust pro-inflammatory profile, characterized by high productionof pro-inflammatory cytokines and the upregulation of HLA-DR and the co-stimulatory molecules CD40and CD86 which are important for antigen presenting cell (APC) function. This activation is amplified in RA patients. We show also that this mechanism is modulated by the presence of C1q and LL-37 proteins, and didn't required the Toll-like receptor 9 (TLR9). Beyond B cell activation, our findings shed light on the domino effect initiated by NETs. NET-activated B cells subsequently act as APCs and trigger T cell activation, bolstering the adaptive immune response. NET-activated B cells also induce the recruitment andactivation of neutrophils. This potential crosstalk highlights the versatile nature of NETs beyond their conventional role in antimicrobial defense
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Jellison, Evan Robert. "CD4 T Cell-Mediated Lysis and Polyclonal Activation of B Cells During Lymphocytic Choriomeningitis Virus Infection: A Dissertation." eScholarship@UMMS, 2008. https://escholarship.umassmed.edu/gsbs_diss/349.
Анотація:
CD4 T cells and B cells are cells associated with the adaptive immune system. The adaptive immune system is designed to mount a rapid antigen-specific response to pathogens by way of clonal expansions of T and B cells bearing discrete antigen-specific receptors. During viral infection, interactions between CD4 T cells and B cells occur in a dynamic process, where B cells that bind to the virus internalize and degrade virus particles. The B cells then present viral antigens to virus-specific CD4 T cells that activate the B cells and cause them to proliferate and differentiate into virus-specific antibody-secreting cells. Yet, non-specific hypergammaglobulinemia and the production of self-reactive antibodies occur during many viral infections, and studies have suggested that viral antigen-presenting B cells may become polyclonally activated by CD4 T cells in vivo in the absence of viral engagement of the B cell receptor. This presumed polyclonal B cell activation associated with virus infection is of great medical interest because it may be involved in the initiation of autoimmunity or contribute to the long-term maintenance of B cell memory.
In order to directly examine the interactions that occur between T cells and B cells, I asked what would happen to a polyclonal population of B cells that are presenting viral antigens, if they were transferred into virus-infected hosts. I performed these studies in mice using the well-characterized lymphocytic choriomeningitis virus (LCMV) model of infection. I found that the transferred population of antigen-presenting B cells had two fates. Some antigen-expressing B cells were killed in vivo by CD4 T cells in the first day after transfer into LCMV-infected hosts. However, B cells that survived the cytotoxicity underwent a dynamic polyclonal activation manifested by proliferation, changes in phenotype, and antibody production.
The specific elimination of antigen-presenting B cells following adoptive transfer into LCMV-infected hosts is the first evidence that MHC class II-restricted killing can occur in vivo during viral infection. This killing was specific, because only cells expressing specific viral peptides were eliminated, and they were only eliminated in LCMV-infected mice. In addition to peptide specificity, killing was restricted to MHC class II high cells that expressed the B cell markers B220 and CD19. Mice depleted of CD4 T cells prior to adoptive transfer did not eliminate virus-specific targets, suggesting that CD4 T cells are required for this killing. I found that CD4 T cell-dependent cytotoxicity cannot be solely explained by one mechanism, but Fas-FasL interactions and perforin are mechanisms used to induce lysis.
Polyclonal B cell activation, hypothesized to be the cause of virus-induced hypergammaglobulinemia, has never been formally described in vivo. Based on previous studies of virus-induced hypergammaglobulinemia, which showed that CD4 T cells were required and that hypergammaglobulinemia was more likely to occur when virus grows to high titer in vivo, it was proposed that the B cells responsible for hypergammaglobulinemia may be expressing viral antigens to virus-specific CD4 T cells in vivo. CD4 T cells would then activate the B cells. However, because the antibodies produced during hypergammaglobulinemia are predominantly not virus-specific, nonvirus-specific B cells must be presenting viral antigens in vivo.
In my studies, the adoptively transferred B cells that survived the MHC class II-restricted cytotoxicity became polyclonally activated in LCMV-infected mice. Most of the surviving naïve B cells presenting class II MHC peptides underwent an extensive differentiation process involving both proliferation and secretion of antibodies. Both events required CD4 cells and CD40/CD40L interactions to occur but B cell division did not require MyD88-dependent signaling, type I interferon signaling, or interferon γ signaling within B cells. No division or activation of B cells was detected at all in virus-infected hosts in the absence of cognate CD4 T cells and class II antigen. B cells taken from immunologically tolerant donor LCMV carrier mice with high LCMV antigen load became activated following adoptive transfer into LCMV-infected hosts, suggesting that B cells can present sufficient antigen for this process during a viral infection. A transgenic population of B cells presenting viral antigens was also stimulated to undergo polyclonal activation in LCMV-infected mice. Due to the high proportion of B cells stimulated by virus infection and the fact that transgenic B cells can be activated in this manner, I conclude that virus-induced polyclonal B cell activation is independent of B cell receptor specificity. This approach, therefore, formally demonstrates and quantifies a virus-induced polyclonal proliferation and differentiation of B cells which can occur in a B cell receptor-independent manner.
By examining the fate of antigen-presenting B cells following adoptive transfer into LCMV-infected mice, I have been able to observe dynamic interactions between virus-specific CD4 T cells and B cells during viral infection. Adoptive transfer of antigen-presenting B cells results in CD4 T cell-mediated killing and polyclonal activation of B cells during LCMV infection. Studies showing requirements for CD4 T cells or MHC class II to control viral infections must now take MHC class II-restricted cytotoxicity into account. Polyclonal B cell activation after viral infection has the potential to enhance the maintenance of B cell memory or lead to the onset of autoimmune disease.
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Ouedraogo, David Eric. "Exploration du réservoir EBV chez les patients infectés par le VIH : implications pathologiques." Thesis, Montpellier 1, 2013. http://www.theses.fr/2013MON1T001.
Анотація:
Les lymphocytes B mémoires circulants incluant ceux infectés par EBV de façon latente retournent périodiquement vers les territoires lymphoïdes secondaires où ils subissent une différenciation en cellules productrices d'immunoglobulines permettant au virus d'initier la réplication virale. Cependant, le suivi et la gestion de la réactivation de EBV et son association avec des néoplasies lymphoïdes chez les sujets infectés par le VIH restent un sujet de controverse et nécessite une meilleure compréhension des mécanismes impliqués. Dans cette étude, nous avons proposé de nouveaux outils biologiques pour la quantification de l'ADN EBV permettant la discrimination entre le réservoir latent et le cycle lytique du virus. Nous avons montré que la taille de ces réservoirs est étroitement associée à une activation polyclonale plus ou moins importante des cellules B. Nous avons également observé une association entre les marqueurs d'activation immunitaire et de réactivation de EBV avec la survenue de lymphome B. En outre, nous avons décrit l'évolution de gammapathies monoclonales chez des sujets infectés par le VIH sous traitement antirétroviral, et la persistante du pic monoclonal d'immunoglobulines était associée à des charges virales EBV plus élevés. Par conséquent, l'activation des lymphocytes B et subséquemment la réactivation EBV joueraient vraisemblablement les rôles principaux dans la survenue de tumeurs bénignes ou malignes des lymphocytes B au cours de l'infection VIHIt is assumed that circulating memory B cells including those latently infected by EBV return periodically to lymphoid nodes where they are stimulates and undergo differentiation into immunoglobulin-producing cells allowing the virus to initiate viral replication. However, the monitoring and the management of EBV reactivation and it association with lymphoid malignancies in HIV-infected patients are still being controversies and need a better understanding of the probable mechanisms involved. In this study, we proposed novel biological tools for EBV DNA quantification allowing discriminating latent and lytic reservoir. We showed that the EBV reservoir levels are closely associated with the polyclonal B-cell activation. We also observed an association between immune activation and EBV reactivation markers with the occurrence of B-cell lymphoma. Moreover, we described a long term evolution of monoclonal gammapathies in HIV-infected subjects and the persistence of the immunoglobulis monoclonal pike was found to be associated with higher EBV reservoir levels. Therefore, the B-cell activation and subsequently EBV reactivation likely play the main roles on the occurrence of B lymphocytes malignancies during HIV infection
4
Cangiani, Eloísa Elena. "Caracterização do padrão das citocinas e dos isótipos de imunoglobulinas produzidos na Yersiniose experimental murina /." Araraquara : [s.n.], 2005. http://hdl.handle.net/11449/100122.
Анотація:
Resumo: Yersinia enterocolitica é um enteropatógeno que pode levar ao desenvolvimento de artrite reativa. Um dos mecanismos imunomoduladores usados pelos patógenos artritogênicos é a ativação policlonal de linfócitos. O objetivo deste estudo foi verificar se ocorre ativação policlonal de linfócitos B e comparar o padrão isotípico de imunoglobulinas produzidas durante a infecção com Y. enterocolitica O:8 em linhagens de camundongos suscetíveis (BALB/c) e resistentes (C57BL/6), bem como analisar o padrão de secreção de citocinas pró-inflamatórias e regulatórias pelas populações de células T CD4+ e CD8+.Abstract: Yersinia enterocolitica is an enteropathogen that can lead to the development of reactive arthritis. One of the immunomodulating mechanisms used by arthritogenic pathogens is the polyclonal activation of lymphocytes. The objective of this study was to verify if the polyclonal activation of B-lymphocytes occur and to compare the different immunoglobulin (Ig) isotypes produced during the infection with Y. enterocolitica O:8 in susceptible (BALB/c) and resistant (C57BL/6) mice strains. We also analyzed the production of pro-inflammatory and regulatory cytokines in T CD4+ and T CD8+ lymphocytes populations.
Orientador: Beatriz Maria Machado de Medeiros
Coorientador: Iracilda Zeppone Carlos
Banca: Maria Regina D'Império Lima
Banca: Phileno Pinge
Banca: Ângela Maria Victoriano de Campos Soares
Banca: Deise Pasetto Falcão
Doutor
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Cangiani, Eloísa Elena [UNESP]. "Caracterização do padrão das citocinas e dos isótipos de imunoglobulinas produzidos na Yersiniose experimental murina." Universidade Estadual Paulista (UNESP), 2005. http://hdl.handle.net/11449/100122.
Анотація:
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Universidade Estadual Paulista (UNESP)
Yersinia enterocolitica é um enteropatógeno que pode levar ao desenvolvimento de artrite reativa. Um dos mecanismos imunomoduladores usados pelos patógenos artritogênicos é a ativação policlonal de linfócitos. O objetivo deste estudo foi verificar se ocorre ativação policlonal de linfócitos B e comparar o padrão isotípico de imunoglobulinas produzidas durante a infecção com Y. enterocolitica O:8 em linhagens de camundongos suscetíveis (BALB/c) e resistentes (C57BL/6), bem como analisar o padrão de secreção de citocinas pró-inflamatórias e regulatórias pelas populações de células T CD4+ e CD8+.
Yersinia enterocolitica is an enteropathogen that can lead to the development of reactive arthritis. One of the immunomodulating mechanisms used by arthritogenic pathogens is the polyclonal activation of lymphocytes. The objective of this study was to verify if the polyclonal activation of B-lymphocytes occur and to compare the different immunoglobulin (Ig) isotypes produced during the infection with Y. enterocolitica O:8 in susceptible (BALB/c) and resistant (C57BL/6) mice strains. We also analyzed the production of pro-inflammatory and regulatory cytokines in T CD4+ and T CD8+ lymphocytes populations.
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Landgraf, Taise Natali. "Receptor de aerobactina férrica de Escherichia coli - IutA: um novo antígeno T-independente do tipo 1." Universidade de São Paulo, 2012. http://www.teses.usp.br/teses/disponiveis/17/17147/tde-30072012-174116/.
Анотація:
Alguns fatores de virulência em bactérias de microbiota normal, tais como sideróforos moléculas captadoras de ferro e determinadas fímbrias, possibilitam que esses microorganismos causem infecção quando a colonização ocorre fora de seu habitat normal. Dentre as diferentes espécies bacterianas da microbiota normal com potencial para causar doenças, como as infecções do trato urinário (ITUs), destaca-se Escherichia coli. Certas cepas dessa espécie bacteriana apresentam um plasmídeo (pColV) que contém um gene que codifica IutA, o receptor para a aerobactina férrica, que é um sideróforo frequentemente associado às ITUs. Recentemente, nosso grupo estabeleceu que IutA apresenta a capacidade de induzir proliferação de linfócitos B. Neste trabalho, objetivamos identificar as moléculas e os mecanismos que modulam a proliferação de linfócitos B induzida por IutA recombinante (rIutA) de E. coli. Para avaliar se a proliferação era dependente de outras células, foram realizados ensaios de proliferação de células B marcadas com CFSE utilizando o sobrenadante de macrófagos ou células dendríticas estimulados com rIutA, por 24 horas, ou coculturas em placas de transwell. As análises desses ensaios revelaram que a proliferação das células B induzida por rIutA é dependente de moléculas liberadas por células acessórias, ou seja, ocorre de forma indireta. Os resultados dos ensaios utilizando células deficientes da molécula adaptadora MyD88 mostraram dependência da sinalização por essa molécula nos linfócitos B, mas não nas células acessórias, para que ocorresse a proliferação. Posteriormente, os ensaios in vitro utilizando células de animais deficientes para TLR4, TLR2 e IL-33R mostraram que a sinalização por esses receptores é dispensável. Contrariamente, a utilização do antagonista do receptor de IL-1 reduziu significativamente a proliferação de células B tratadas com esse antagonista. Além disso, identificamos que rIutA leva à expressão de IL-1 em macrófagos e células dendríticas estimuladas com essa proteína. Assim, nossos resultados sugerem que rIutA de E. coli induz a proliferação policlonal de linfócitos B de maneira independente de células T, por um mecanismo mediado por células acessórias, como macrófagos e células dendríticas. Embora não identifiquemos o receptor macrofágico ou das células dendríticas a qual rIutA se liga, sugerimos que a ação de rIutA sobre essas células induz a produção de IL-1 que age sobre seu receptor em células B, induzindo-as a proliferação. Esses resultados abrem perspectivas de estudo de IutA como molécula estimuladora do tecido linfóide associado a mucosa, assim como evasina de E. coli patogênicas.Indigenous bacteria may contain some virulence factors, such as siderophores iron chelator molecules and fimbriae, that allow these microorganisms to become pathogens in sites others than their normal habitat. Among the different indigenous bacterial species in the gut, Escherichia coli is one with potential to cause infections, mainly urinary tract infection (UTI). Certain strains of E. coli have a plasmid (pColV), which encode ferric aerobactin outer membrane receptor, IutA, often associated with UTI. Our group has recently described IutA as an inducer of B cell proliferation. Here, we identify the molecules and mechanisms that modulate the proliferation of B lymphocytes induced by recombinant IutA (rIutA) from E. coli. To determine whether the B cell proliferation induced by rIutA is dependent on other cell, we carried out assays with CFSE-labeled B cells cocultured separately with macrophages or dendritic cells stimulated with rIutA using transwell membranes or incubated with conditioned medium from these cells. The analysis of the results showed that rIutA indirectly induced the proliferation of B cells in a manner dependent on molecules released by accessory cells. When we analyzed the ability of rIutA in inducing proliferation of cells from mice deficient in adapter molecule MyD88, we found that this signaling molecule is crucial for signaling induced by rIutA in B cells, but not in accessory cells. A similar analysis with cells from mice deficient in Toll like receptor (TLR) 4, TLR2 or inteukin (IL-) 33 receptor revealed that these receptors were not required for rIutA signaling of any tested cells. Conversely, the pretreatment of the B cells with IL-1 receptor antagonist significantly decreased the proliferation of these cells in response to conditioned medium from cultures of IutAstimulated macrophages. Moreover, we determined that rIutA induced the expression of IL-1 in macrophages and dendritic cells stimulated with IutA. Altogether, our results suggest that IutA from E. coli induces polyclonal B-cell proliferation independently of T cells in a mechanism mediated by accessory cells such as macrophages and dendritic cells. Although the IutA-binding receptors from macrophages and dendritic cells have not been identified, we suggested that rIutA induces these cells to produce IL-1, which in turns acts on its receptor on B cells, triggering proliferation. These results open perspectives for studying IutA as a molecule that stimulates the mucosa-associated lymphoid tissue and as an immune-evasion molecule from pathogenic E. coli.
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Silva, Joselli Santos. "Desestruturação da polpa branca do baço na leishmaniose visceral canina: células e citocinas envolvidas." reponame:Repositório Institucional da FIOCRUZ, 2014. https://www.arca.fiocruz.br/handle/icict/7489.
Анотація:
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Joselli Silva. Desestruturação da polpa... 2014.pdf: 6952851 bytes, checksum: 512840eb0cc488e4f61742ce875c4837 (MD5)Made available in DSpace on 2014-04-03T13:38:30Z (GMT). No. of bitstreams: 1 Joselli Silva. Desestruturação da polpa... 2014.pdf: 6952851 bytes, checksum: 512840eb0cc488e4f61742ce875c4837 (MD5) Previous issue date: 2014
Fundação Oswaldo Cruz. Centro de Pesquisa Gonçalo Moniz. Salvador, BA, Brasil / Universidade Federal da Bahia. Faculdade de Medicina da Bahia. Salvador, BA, Brasil
A leishmaniose visceral está associada às alterações arquiteturais esplênicas e redistribuição de populações celulares envolvidas na resposta imunológica. Os objetivos desta tese foram estudar a desestruturação da polpa branca do baço na leishmaniose visceral canina e quais as células e citocinas envolvidas nesse processo. Para isso, amostras de baços de cães de uma área endêmica para LV foram agrupadas em três categorias: TIPO1-CONT ou TIPO1-SIA (cães não infectados ou sem infecção ativa e com polpa branca organizada), TIPO1-INF (cães infectados com polpa branca organizada) e TIPO3-INF (cães infectados com polpa branca desorganizada). No capítulo 2 e 3, as secções de baço foram marcadas através de imunoistoquímica com anticorpos anti-CD3 (linfócitos T), anti-CD79-α (linfócitos B), anti-S100 (célula dendrítica folicular), anti-Ki-67 (células em proliferação), anti-IgG e anti-IgM (plasmócitos secretores de IgA, IgG e IgM). Foram estimadas as densidades de todas as populações celulares através de morfometria. As expressões de citocinas e quimiocinas foram avaliadas através de RT-PCR em tempo real. A ativação policlonal de células B e hipergamaglobulinemia foram avaliadas por ELISA e eletroforese de proteínas séricas. No capítulo 2, foi visto que a densidade de linfócitos B foi maior nos folículos e na zona marginal dos animais com baço TIPO1 do que nos dos animais com baço TIPO3 (teste de Mann-Whitney P < 0,02). Os números de células proliferantes, células B e células dendríticas foliculares foram menores em animais de baço TIPO3. A expressão da quimiocina CXCL13 foi maior nos animais com baço TIPO 1 (teste de Mann-Whitney, P < 0,02). No capítulo 3, foi visto que a plasmocitose foi maior em animais de baço TIPO3 do que nos animais com baço TIPO1 (Teste qui-quadrado, P < 0,04). A densidade de plasmócitos secretores de imunoglobulina do isotipo IgG foi maior na polpa vermelha de animais com baço TIPO3 (Teste Man-Whitney, P <0,05). Em geral, observou-se uma tendência de maior densidade de plasmócitos secretores de imunoglobulinas dos isotipos IgM e IgG nos animais de baço TIPO3 em comparação com animais do baço TIPO1. Animais de baço TIPO3 apresentam maiores níveis séricos de proteína gamaglobulina e também uma maior expressão das citocinas BAFF e APRIL e da quimiocina CXCL12, que estão envolvidas no processo de ativação e homing de plasmócitos. No capítulo 4 foi visto que uma região de aproximadamente 1.28Mb do cromossomo 8 canino foi encontrada com os segmentos gênicos VH, DH e JH. As principais conclusões obtidas nesse estudo foram que a redistribuição de populações celulares do baço, especialmente de linfócitos B, células dendríticas foliculares e plasmócitos estão relacionada com a desorganização do tecido esplênico e com a expressão anômala de CXCL13, CXCL12, BAFF e APRIL, que são citocinas e quimiocinas envolvida com a organização do tecido esplênico, ativação e homing de plasmócitos. A ativação policlonal, a hipergamaglobulinemia e a diglobulinemia são também relacionadas com a desorganização do baço. As regiões variáveis (VH), diversidade (DH) e de junção (JH) da cadeia pesada de imunoglobulina são compostos de noventa e dois, dez e nove genes obtidos na linha germinativa canina, respectivamente.
Visceral leishmaniasis is associated with splenic architectural changes and redistribution of cell populations involved in the immune response. The objectives of this thesis was to study the disruption of the white pulp of the spleen in canine visceral leishmaniasis and which cells and cytokines are involved in this process. For this, samples of spleens of dogs from an endemic area for VL were grouped into three categories: TYPE1-CONT or TYPE1-NIF (non-infected dogs or without active infection with organized white pulp), TYPE1-INF (infected dogs with pulp organized white) and TYPE3-INF (infected animals with disorganized white pulp). In Chapter 2 and 3 the spleens sections were stained by immunohistochemistry with anti-CD3 (T lymphocytes), anti-CD79 (B lymphocytes), anti-S100 (follicular dendritic cells), anti-Ki-67 (cells proliferation), anti-IgG and anti-IgM (plasma cells). The number and distribution of all cell populations were estimated by morphometry. The expressions of cytokines and chemokines were assessed by real time RT-PCR. The polyclonal B cell activation and hypergammaglobulinemia were evaluated by ELISA and serum protein electrophoresis. In chapter 2, it was seen that the density of B lymphocytes was higher in the marginal zone and follicles of animals with spleen TYPE1-INF than animals with the spleen TYPE3-INF (Mann -Whitney test P < 0.02). The numbers of proliferating cells, B cells and follicular dendritic cells was lower in animals of TYPE3-INF. The expression of the chemokine CXCL13 was higher in the spleen of animal with the spleen TYPE 1 (Mann-Whitney, P < 0.02). No difference was observed in the expression of other cytokines compared between the two groups of animals. In chapter 3, it was seen that the plasma cells was higher in animals with spleen TYPE 3 than in animals with spleen TYPE1 (Chi-square test, P < 0.04). The density of plasma cells secreting the isotype IgG was higher in the red pulp of spleen of animals TYPE3 (Man-Whitney test, P < 0.05). In general, there was a trend toward higher density of plasma cells secreting the immunoglobulin of isotype IgM and IgG in the spleen of animals with spleen TYPE3-INF in comparison to animal’s spleen TYPE1. Animals with spleen TYPE3 have higher levels of serum gamma globulin protein as well as increased expression of citokines, BAFF and APRIL and the chemokine CXCL12 that are involved in the activation and homing plasma cells. The main conclusions of this study were that the redistribution of cell populations of the spleen, especially B lymphocytes, follicular dendritic cells and plasma cells (characterized by intense plasmacytosis) are related to the disorganization of the splenic tissue and aberrant expression of CXCL13, CXCL12, BAFF and APRIL, which are cytokines and chemokines involved in the organization of the splenic tissue, activation of B cells and plasma cell homing. The polyclonal activation, hypergammaglobulinemia and diglobulinemia are also related to the structural disorganization of the splenic lymphoid tissue. In addition, it was concluded that the variable regions (VH), the diversity (DH) and junction (JH) immunoglobulin heavy chain are composed of ninety-two, ten and nine genes that have been obtained in canine germline.
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Chamond, Nathalie. "Quand un mitogène est une enzyme. ." Paris 6, 2003. http://www.theses.fr/2003PA066048.
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Leclercq, Lise. "Analyse du mode d'action du lymphocyte T "helper" : son rôle dans les phases précoces de l'activation de la cellule B et sa contribution à la régulation isotypique." Paris 7, 1985. http://www.theses.fr/1985PA077058.
Анотація:
Lors d'une stimulation par un antigène protéique soluble, les lymphocytes B reconnaissent l'antigène grâce à leurs immunoglobulines (Ig) de surface et collaborent avec des lymphocytes T helper (Th) également spécifiques de cet antigène. Ces interactions cellulaires complexes conduisent la cellule B à produire des anticorps qui représentent la forme soluble de l'Ig de surface. Bien que tous dirigés contre l'antigène, ces anticorps peuvent néanmoins appartenir à différentes classes que l'on appelle isotypes et qui se distinguent par la nature de leur région constante. Notre travail réalisé dans un modèle murin utilisant des clones de lymphocytes Th spécifiques d'un antigène synthétique, le GAT (poly (G1u60 Ala30 Tyr ¹º)), a tenté d'analyser le mode d'action du lymphocyte Th, en particulier son rôle dans les phases précoces de l'activation de la cellule B et sa contribution à la régulation isotypique. Après avoir testé différents clones de lymphocytes Th pour leur capacité à induire une stimulation polyclonale de lymphocytes B vierges, nous avons concentré nos efforts sur le clone le plus actif, appelé 52. 3. Nous avons préparé du surnageant (SN) de culture du clone 52. 3 activé et montré que les lymphocytes B au repos, syngéniques ou allogéniques, prolifèrent en présence de ce SN et en l'absence de tout autre stimulus tel que celui délivré par des anticorps anti-Ig. Par cytométrie de flux, nous avons démontré qu'après stimulation avec du SN du clone 52. 3, la quasi-totalité des lymphocytes B hyperexpriment les antigènes Ia, augmentent de taille (30% d'entre eux devenant blastiques) et passent de G₀ en G₁, mais que seuls 20% d'entre eux atteignent les phases S et G₂/M du cycle cellulaire. Ces résultats nous ont conduits à postuler l'existence dans le SN d'une lymphokine agissant sur les lymphocytes B au repos en provoquant leur passage du stage G₀ au stade G₁ du cycle cellulaire et ceci d'une manière qui n'est pas restreinte par les gènes du complexe majeur d'histocompatibilité (CMH). Après stimulation avec le clone de lymphocytes Th 52. 3, des lymphocytes B spléniques IgM⁺ IgG⁻ (isolés par passage au trieur de cellules) sont capables de produire, en plus de l'isotype dominant IgM, des Ig appartenant aux différentes sous-classes d'IgG (avec une nette prédominance des IgG1). Des résultats analogues concernant la sécrétion des IgA ont été obtenus avec des lymphocytes IgM⁺ IgA⁻ isolés par adhérence sur une boîte recouverte d'anticorps anti-IgA. La stimulation de cellules B IgM⁺ IgG⁻ IgA⁻ par du SN du clone 52. 3 induit une réponse plus faible que celle induite par les cellules 52. 3 elles-mêmes, mais elle conduit néanmoins à une production des isotypes IgM, IgG et IgA. Parmi l'isotype IgG la sous-classe IgGi est dominante. Les expériences conduites sur des cellules B IgM⁺ IgG⁻ IgA⁻ semblent indiquer que des cellules Th spécifiques d'isotype ne sont pas indispensables pour qu'une cellule B primaire stimulée par une cellule Th spécifique d'un antigène produise des anticorps d'un isotype autre que IgM.
Книги з теми "Activation polyclonal":
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Carlino, Joseph A. Pregnancy-associated growth factor (PAGF): A T-dependent polyclonal activator of human lymphocytes. 1986.
Частини книг з теми "Activation polyclonal":
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Azim, T., J. Golay, K. Lam, and D. H. Crawford. "Polyclonal Activation of B Lymphocytes after EB Virus Infection." In Epstein-Barr Virus and Human Disease, 331–32. Totowa, NJ: Humana Press, 1987. http://dx.doi.org/10.1007/978-1-4612-4590-2_72.
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Sultzer, Barnet M. "Polyclonal Lymphocyte Activation by M. tuberculosis and Its Products." In Infectious Agents and Pathogenesis, 277–304. Boston, MA: Springer US, 1988. http://dx.doi.org/10.1007/978-1-4684-5418-5_13.
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Tzioufas, A. G., N. Talal, and H. M. Moutsopoulos. "Sjögren’s Syndrome: From Polyclonal B Cell Activation to Monoclonal B Cell Proliferation." In Immunology of the Connective Tissue Diseases, 335–53. Dordrecht: Springer Netherlands, 1994. http://dx.doi.org/10.1007/978-94-011-1432-5_16.
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Greco, Raffaella, and Dominique Farge. "CART Cells and Other Cell Therapies (ie MSC, Tregs) in Autoimmune Diseases." In The EBMT Handbook, 837–48. Cham: Springer International Publishing, 2024. http://dx.doi.org/10.1007/978-3-031-44080-9_93.
Анотація:
AbstractAuto-immune diseases (AD) are heterogeneous conditions, characterized by polyclonal activation of the immune system with a defect of B or T lymphocyte selection and altered lymphocytic reactions to auto-antigens components (Burnet 1959a, b), although it is rare to identify a single antigenic epitope. The native immune system and its tissue environment play an important role to determine if exposure to a given antigen will induce an immune response or tolerance or anergy. The role of the genes coding for the major histocompatibility system molecules, but also of many other genes, is important in the regulation of the immune response, although this does not explain all the observed phenomena during loss of tolerance (Matzinger 1994; Rioux and Abbas 2005).
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Klinman, Dennis M., Akira Shirai, and Yoshiaki Ishigatsubo. "Polyclonal B Cell Activation and B Cell Cross-Reactivity During Autoantibody Production in Systemic Lupus Erythematosus." In Advances in Experimental Medicine and Biology, 115–23. Boston, MA: Springer US, 1994. http://dx.doi.org/10.1007/978-1-4615-2427-4_12.
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Mayer, Lloyd. "Factors Generated by Human T-Cell Hybridomas Regulate B-Cell Activation, Polyclonal Differentiation, and Isotype Expression." In Human Hybridomas and Monoclonal Antibodies, 401–18. Boston, MA: Springer US, 1985. http://dx.doi.org/10.1007/978-1-4684-4949-5_24.
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Karulin, Alexey Y., Melinda Katona, Zoltán Megyesi, Greg A. Kirchenbaum, and Paul V. Lehmann. "Artificial Intelligence-Based Counting Algorithm Enables Accurate and Detailed Analysis of the Broad Spectrum of Spot Morphologies Observed in Antigen-Specific B-Cell ELISPOT and FluoroSpot Assays." In Methods in Molecular Biology, 59–85. New York, NY: Springer US, 2024. http://dx.doi.org/10.1007/978-1-0716-3690-9_5.
Анотація:
AbstractAntigen-specific B-cell ELISPOT and multicolor FluoroSpot assays, in which the membrane-bound antigen itself serves as the capture reagent for the antibodies that B cells secrete, inherently result in a broad range of spot sizes and intensities. The diversity of secretory footprint morphologies reflects the polyclonal nature of the antigen-specific B cell repertoire, with individual antibody-secreting B cells in the test sample differing in their affinity for the antigen, fine epitope specificity, and activation/secretion kinetics. To account for these heterogeneous spot morphologies, and to eliminate the need for setting up subjective counting parameters well-by-well, CTL introduces here its cutting-edge deep learning-based IntelliCount™ algorithm within the ImmunoSpot® Studio Software Suite, which integrates CTL’s proprietary deep neural network. Here, we report detailed analyses of spots with a broad range of morphologies that were challenging to analyze using standard parameter-based counting approaches. IntelliCount™, especially in conjunction with high dynamic range (HDR) imaging, permits the extraction of accurate, high-content information of such spots, as required for assessing the affinity distribution of an antigen-specific memory B-cell repertoire ex vivo. IntelliCount™ also extends the range in which the number of antibody-secreting B cells plated and spots detected follow a linear function; that is, in which the frequencies of antigen-specific B cells can be accurately established. Introducing high-content analysis of secretory footprints in B-cell ELISPOT/FluoroSpot assays, therefore, fundamentally enhances the depth in which an antigen-specific B-cell repertoire can be studied using freshly isolated or cryopreserved primary cell material, such as peripheral blood mononuclear cells.
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Plagemann, Peter G. W., Quentin A. Jones, and William A. Cafruny. "Polyclonal Activation of B Cells by Lactate Dehydrogenase-Elevating Virus is Mediated by N-Glycans on the Short Ectodomain of the Primary Envelope Glycoprotein." In Advances in Experimental Medicine and Biology, 375–84. Boston, MA: Springer US, 2001. http://dx.doi.org/10.1007/978-1-4615-1325-4_56.
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Beris, Photis, and Francis A. Waldvogel. "Hematologic Alterations in Infectious Disease Patients." In Clinical Infectious Diseases, 121–32. Oxford University PressNew York, NY, 1998. http://dx.doi.org/10.1093/oso/9780195081039.003.0013.
Анотація:
Abstract Defense of the host against infectious agents covers a large spectrum of mechanisms, which include: acute inflammatory reactions, activation of complement, activation of macrophages, activation of granulocytes, polyclonal activation of some T-cell subsets, and T cell-dependent or T cell-independent polyclonal B cell activation. Cellular and humoral blood elements are involved in protection against infection and, when this is not possible, in its eradication or control.
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Silman, Alan J., and Marc C. Hochberg. "Systemic lupus erythematosus*." In Epidemiology of the Rheumatic Diseases, 163–91. Oxford University PressNew York, NY, 1993. http://dx.doi.org/10.1093/oso/9780192623560.003.0007.
Анотація:
Abstract Systemic lupus erythematosus (SLE) is a multisystem disorder characterized by an abundance of immunologic abnormalities including loss of self-tolerance, polyclonal B-lymphocyte activation and the production of auto-antibodies to a variety of cellular constituents. The clinical features of SLE are well described and include, in descending order of frequency, constitutional symptoms (malaise, fever, and weight loss), skin and mucous membrane involvement, arthritis and/or arthralgia, pleurisy and/or pericarditis, renal involvement, central nervous system involvement, Raynaud’s phenomenon, peripheral vasculitis, and inflammatory myositis.
Тези доповідей конференцій з теми "Activation polyclonal":
1
Kazama, M., H. Ishii, J. Tsubouchi, M. Nakano, N. Hiramoto, T. Abe, and P. W. Majerus. "PREPARATION OF ANTI-HUMAN THROMBOMODULIN ANTIBODIES AND THEIR APPLICATION FOR STUDY ON PLASMA THROMBOMODULIN." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643962.
Анотація:
Thrombomodulin is an endothelial cell membrane protein that is cofactor required for rapid activation of plasma protein C. Recently, thrombomodulin was found also in plasma in normal subject. However, the information of the soluble thrombomodulin in plasma is very poor. We now report the preparation of polyclonal and monoclonal anti-human thrombomodulin and their application for study on plasma thrombomodulin.Thrombomodulin was extracted from human placenta by 0.5% of Triton X-100 and purified by DIP-thrombin column chromatography. Polyclonal anti-thrombomodulin antibody was obtained from rabbit serum. The three types of monoclonal anti-human thrombomodulin antibodies were obrained from hybrid cell of BALB/C spleen cell and SP2 mouse myeloma cell. The type 1 monoclonal antibody inhibited the thrombomodulin activity. The type 2 of the antibody did not inhibit the activity. The type 3 of antibody cross reacted with rabbit lung thrombomodulin. The IgGs of these antibodies were separated by protein A Sepharose. The plasma thrombomodulin was separated using polyclonal anti-thrombomodulin IgG Sepharose. The apparent molecular weight of plasma thrombomodulin was estimated by immunoblot analysis using monoclonal anti-thrombomodulin IgG. When run with mercaptoethanol, plasma thrombomodulin migrated mainly at Mr=85,000 against Mr=105,000 of tissue thrombomodulin. The plasma thrombomodulin had an apparent Km for 1 nM compared with 0.3nM for tissue thrombomodulin. The apparent Km for protein C was same between tissue and plasma thrombomodulin.
2
Rickles, F. R., W. W. Hancock, K. Kobzik, N. Hogg, and C. O’Hara. "THE DISTRIBUTION OF CROSS-LINKED FIBRIN IN HUMAN LUNG CARCINOMA PARALLELS THAT OF ACTIVATED HOST MONONUCLEAR LEUKOCYTES: IMMUNO-HISTOLOGIC STUDIES WITH MONOCLONAL ANTIBODIES." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643669.
Анотація:
Previous immunohistologic studies of human lung carcinoma, using polyclonal antibodies to antigens shared between fibrinogen (FGN) and fibrin (FB), showed that FGN/FB were associated withtumor cells. These findings were interpreted as evidence of the presence of tumor-associated procoagulant activity(PCA). Wecompared the distribution of coagulation-associated proteins in 16 casesof human carcinoma of the lungofvarying histologic types, using polyclonal antibodies to FGN/FB and monoclonal antibodies (mAb) to cross-linked fibrin (XL-FB;UC-45), fibronectin (FN;PHM13), factor VIII (vWF:Ag)and a tissue factor-related antigen(TF:RAg;A1 -3)- Host mononuclear leukocytes were identifiedusing various mAb toT cells and macrophages, and studied for their expression of receptorsfor interleukin-2 (IL-2R). Positive resultsare summarizedIn addition, studies of the mononuclearcells adjacent to tumors in 12/12 casesshowed the presence of tumor-associated macrophages, 10/11 showed T cells,mainly T8+, and A/5 showed corresponding expression of IL-2R, suggesting cell activation.The use of highly specific mAb showed that XL-FB is actually more selectively distributed than is found using polyclonal antisera to FGN/FB, and indeed XL-FB was largely confined to those areas adjacent to tumors which are rich in mononuclearcells. These findings suggest that fibrin deposits in human carcinomasof the lung may be due todevelopment of PCA by activated host mononuclear cells, rather than tumor cells.This lack of XL-FB on tumor cellsinspite of A1- 3 binding suggests that TF:RAg may not be available on the tumor cell surface for the activation of clotting. Further studies are neededto define the functional capacity of PCA molecules on tumor cells and tumor-associated mononuclear cells in situ.
3
Gordon, Stuart, Bonnie Sloane, Phil Cavanugh, Barbara Cross, Kenneth Honn, and Mohanathasan Chelladurai. "PURIFICATION AND CHARACTERIZATION OF TWO PROCOAGULANTS FROM WALKER 256 CARCINOSARCOMA TUMORS,." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643666.
Анотація:
Activation of the coagulation system bytumor cells may play an important role in tumor growth and metastases. Becauseprocoagulant activities have been identified in different tumor cells by different investigators, effective comparison of these activities has been difficult. Therefore, we purified and characterized two different procoagulant proteins from the same Walker 256 tumors. The first procoagulant activity/platelet aggregating activity (PCA/PAA) was purified from a 1% CHAPS detergent extract oftumor homogenate followed by (NH4)2SO4 fractionation, anion exchange and hydrophobic chromatography. The protein had a molecular weight of 58,000, required phospholipid and an intact coagulation pathway from factor X through fibrinogen for activity, but did not require factors VII or IX forits procoagulant activity. The procoagulant activity was not inhibited by 5mMphenyl-methyl sulfonyl fluoride, iodoacetamide or phenanthroline; there was noevidence of proteinase activity. The PAA was due to thrombin generation during coagulation. The second procoagulant,cancer procoagulant (CP), was extracted from tumors in barbital buffer (pH 7.4) without detergent, purified by immunoaffinity (using a polyclonal goat antibody to CP from V2 carcinoma) and mercurial-benzoate affinity chromatography. CP had a molecular weight of 68,000, an isoelectric point of 4.8 and initiated coagulation by directly activating factor X in the coagulation system. CP was inhibited by Hg++ and iodoacetamide, cysteine proteinase inhibitors. The purified CP formed an immunodiffusion precipitin band against the polyclonal anti-CP goat antibody. Thus, thepurified CP had the same physicochemical, enzymatic and immunologic propertiesas CP from rabbit V2 carcinoma. Neither procoagulant had the properties of tissue factor. These results suggest that there aretwo distinct procoagulant activities inWalker 256 and that both may contributeto the coagulation abnormalities that are associated with tumor growthand metastases.
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Veloso, D., M. Shapira, F. Kueppers та R. W. Colman. "MONOCLONAL ANTIBODY 13G11 RECOGNIZES PREKALLIKREIN, KALLIKREIN AND COMPLEXES OF KALLIKREIN WITH,C1-INHIBITOR AND. α2-MACR0GL0BULIN". У XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1642901.
Анотація:
Abnormal prekallikrein (PK) levels in plasma can be due to decreased biosynthesis or increased activation either by surface-activated factor XIIa (e.g., in septicemia) or by other proteases (e.g., in pancreatites). To study the products of activation of PK in plasma, intact normal plasma and plasma exposed to either activating surfaces or factor XII fragment, was immunoblotted from SDS-gels. MAb 13G11 which recognizes purified PK, kallikrein (KAL) and the complexes of KAL with Cl-inhibitor (Cl-Inh) and α2macroglobulin (α2M) formed from purified proteins detected a doubLet (88- and 85-kDa) which comigrated with PK and KAL but was not visible in PK-deficient plasma. Transfer of either PK in normal plasma (25-125 ng) or KAL (50-300 ng) added to PK-deficient plasma was proportional to the amount of protein applied to the SDS-gels. Activation of plasma decreased the intensity of the PK bands with the formation of new bands with molecular weights similar to those of KAL-Cl-Inh and KAL-α2M. Identity was confirmed by MAb 4C3 (reacts with KAL-Cl-In, not with KAL) and a polyclonal antibody to α2M. Increase of incubation temperature from 24 to 37 increased KAL-Cl-Inh and decreased KAL-α2M. Addition of an excess of a2M before surface activation caused an increase of KAL-α2M complex and a decrease of KAL-Cl-Inh. Addition of an excess of Cl-Inh increased KAL-Cl-Inh and decreased KAL-α2M. In addition, activation of Cl-Inh-deficient plasma showed lower KAL-Cl-Inh and higher KAL-a2M than those when normal plasma was activated. When the deficient plasma was treated with CH3NH2 to inactivate α2M, an increase at KAL position was observed since no inhibitors were active. These studies indicate that 13G11 will be useful to detect changes in the distribution of PK, KAL, KAL-Cl-Inh and KAL-α2M associated with abnormal activation of PK and/or abnormal availability of inhibitors in disease.
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Oft, Martin, Aung Naing, Jeffrey R. Infante, Kyriakos P. Papadopoulos, Ivan H. Chan, Cong Shen, Navneet P. Ratti, et al. "Abstract A016: PEGylated IL-10 (pegilodecakin) induces systemic immune activation, CD8+ T-cell invigoration and polyclonal T-cell expansion in cancer patients." In Abstracts: Fourth CRI-CIMT-EATI-AACR International Cancer Immunotherapy Conference: Translating Science into Survival; September 30 - October 3, 2018; New York, NY. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/2326-6074.cricimteatiaacr18-a016.
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Piotrowicz, Randolph S., Kenneth M. Yamada, and Kunicki J. Kunicki. "HUMAN PLATELET GLYCOPROTEIN Ic-IIa IS AN ACTIVATION-INDEPENDENT FIBRONECTIN RECEPTOR." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643911.
Анотація:
Human platelets express the membrane glycoprotein (GP) heterodimer GPIIb-IIIa, which functions as an activation-dependent fibronectin (Fn) receptor. We have immunopurified the components of an activation-independent Fn receptor (FR) from human platelets employing a well-characterized rabbit polyclonal antibody raised against the beta chain of the chicken embryo fibroblast (CEF) FR (anti-band 3). This antibody crossreacts with antigen(s) expressed on both chicken thrombocytes and human platelets and inhibits the binding of both normal and thrombasthenic platelets (lacking GPIIb-IIIa) to Fn-coated surfaces in the absence of platelet activation.A monoclonal antibody directed against GPIIb-IIIa (AP2) partially inhibits the adhesion of normal platelets to Fn, but the combination of AP2 and anti-band 3 results in a level of inhibition greater than that obtained with either antibody alone. Thus, the presence of the FR alone is sufficient for the observed normal to enhanced binding of thrombasthenic platelets to Fn, whereas adhesion of normal platelets involves the synergistic action of the FR and GPIIb-IIIa. The adhesion of platelets to Fn mediated by the FR is inhibited by the tetrapeptide RGDS.Immunopurified FR appears to be a complex of two proteins: an alpha chain with an apparent molecular weight of 155/130 KD (nonreduced/reduced) and a beta chain with an apparent molecular weight of 125/147 KD. The alpha chain is composed of two subunits, dissociated by reduction, with electrophoretic mobilities identical to platelet glycoproteins previously designated lea and IcB. The beta chain comigrates with that platelet glycoprotein known as GPIIa. In an immunoblot assay, anti-band 3 binds to GPIIa but not to GPIc. The fact that anti-band 3 iramunoprecipitates both GP therefore suggests that they exist in a complex.Our findings establish GPIc-IIa as yet another platelet glycoprotein receptor complex and pave the way for future studies of the relative role of GPIIb-IIIa and GPIc-IIa in the adhesion of platelets to physiologic surfaces.
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Lindon, J. N., L. Kushner, E. Shiba, and E. W. Salzman. "PLATELET ADHESION ON SYNTHETIC SURFACES PRETREATED WITH DILUTED PLASMA IS DETERMINED BY THE SURFACE CONCENTRATION OF "NATIVE" FIBRINOGEN." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643551.
Анотація:
Platelet adhesion and activation on synthetic surfaces are thought to require the prior adsorption of fibrinogen. We have reported that platelet activation by polyalkyl methacrylates (measured in bead columns exposed to flowing blood) is better correlated with the concentration of conformationally unaltered, "native" (recognizable by radiolabeled antifibrinogen antibodies) bound fibrinogen than with total bound fibrinogen (measured with radiolabeled fibrinogen) following exposure of the surfaces to purified fibrinogen in solution or to diluted blood plasma (Blood 68:355, 1986). We now report that adhesion of washed platelets to polybutyl methacrylate (PBMA; approx. 20% retention in bead columns), was unaffected by preincubation of the surface with whole plasma but was increased significantly by precoating with diluted plasma, with maximum retention (approx. 65%) occurring with plasma diluted 3000-fold. Upon exposure of PBMA to various plasma dilutions the surface concentration of antibody-detectable fibrinogen, but. not of total surface-bound fibrinogen, was correlated with the activation of washed platelets by such pretreated surfaces, With maximal platelet reactivity occurring in columns precoated with the plasma dilution (1:3000) that produced the highest concentration of "native" surface-bound fibrinogen. The plasma dilution that gave maximum total fibrinogen adsorption (100-fold dilution) was not correlated with the concentration of antibody-detectable fibrinogen. Fab fragments of polyclonal anti-fibrinogen antibodies totally prevented platelet activation by PBMA surfaces precoated with diluted plasma. It appears that participation of surface-bound fibrinogen in platelet activation on some artificial surfaces requires that fibrinogen be adsorbed in a conformationally "native" state, presumably thereby permitting multivalent, cooperative interactions with GP IIb/IIIa receptors on platelets.
8
Bartsch, P., A. Haeberli, and P. W. Straub. "NORMAL FIBRINOPEPTTDE A (FPA) AND ELEVATED FIBRINOGEN DEGRADATION PRODUCTS AFTER LONG DISTANCE RUNNING." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643132.
Анотація:
Physical exercise leads to a shortening of activated partial thrcnboplastin time (PIT) and euglobulin lysis time (ELT). Whether this activation causes in-vivo thrombin and plasmin action remains controversial however. 19 well trained long distance runners were examined 25 min (range 5-53) after termination of a 100 km race (post-race values) run in 577 min (457-755) and 5 days later after at least one day without physical exercise (control values). FPA, platelet factors and fibrin (ogen) split products (fragment E and BB 15-42) were measured with radioimnunoassays. ELT was assessed before and after venous occlusion (VO). The table gives mean values ±SD:Thrombin time, platelet count, platelet factor 4 and haematocrit did not change significantly. FPA was normal in all post-race samples and did not correlate significantly with the time lag between arrival and blood sampling, indicating that activation of blood coagulation in exhaustive physical exercise of long duration does not lead to in-vivo fibrin formation. Activation of fibrinolysis, however, results in circulating plasmin activity as demonstrated by the elevation of the fibrin (ogen) degradation products fragment E and BB 15-42. Since the polyclonal antibodies used in the latter assay crossreact with BB 1-42, these results alone do not allow to jjdge whether plasmin degrades fibrin or fibrinogen. However, lack of fibrin formation suggests fibrinogenolysis rather than fibrinolysis.
9
Gralnick, H. R., L. M. Magurder, K. Hansmann, M. Vail, G. Marti, R. McEver, and S. Williams. "THE SURFACE EXPRESSION OF ALPHA GRANULE PROTEINS FOLLOWING THROMBIN STIMULATION." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643859.
Анотація:
We have studied the platelet glycoproteins (GP) GPIb and the GPIIb/IIIa and the expression of alpha granule proteins (AGP) on the platelet (P) surface following thrombin (T) stimulation. The platelets were separated from plasma proteins on a arabinogalactan gradient. The P were stimulated with purified alpha T 0.1u/108p. Either monospecific polyclonal or murine monoclonal antibodies were used to detect the P glycoprotein and AGP. The platelets were analyzed on an EPICS V Flow Cytometer. Resting P had small amounts of AGP (2-8%) present on their surface. Within 1-3 min. after T stimulation significantly increased amounts of PF4 (26%) vWf (8%) Ig (10%) and the 140 kD alpha granule membrane (70%) were present on the P surface. The peak expression of all the AGP occurred within 5 mins. The 140 kD activation protein remained stable over 3-60 mins, in contrast the PF4 and the vWf expression peaked at 5 mins. and then decreased to near baseline levels. The GPIb and GPIIb/IIIa showed different patterns after activation. The GPIb intensity and number of positive cells decreased over time, while the GPIIb/ IIIa increased in flourescent intensity and the number of positive cells. These studies indicate that T stimulation of AGP on the P surface. vWf and P4 have a transient appearance on the P surface while Ig and the 140 kD activation protein both appear to become stable components of the P plasma membrane. This technique of detecting platelet activation is a specific, sensitive, and rapid method.
10
Palabrica, Theresa M., Barbara C. Furie, Marvin A. Konatam, Barbara Brockway, Mart Aronovitz, and Bruce Furie. "IMAGING OF THROMBI USING ANTI-PADGEM ANTIBODIES SPECIFIC FOR ACTIVATED PLATELETS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643955.
Анотація:
PADGEM protein is a platelet-specific alpha grannie membrane protein that is translocated to the plasma membrane during platelet activation and secretion. Monoclonal EC4 and polyclonal anti-PADGEM antibodies are specific for PADGEM on activated platelets. Because PADGEM is internal in unstimulated platelets* these antibodies do not bind to resting platelets. Since activated platelets are concentrated in thrombi, we used radiolabeled anti-PADGEM antibodies to image thrombi in baboons.In vitro: Dacron graft material incubated with thrombin-activated platelet-rich plasma and 131I-KC4, 131I-anti-PADGEM, 131I-nonimmune IgG or 131-BSA bound 95%, 70%, 9% and 1% of the radiolabel, respectively, after exhaustive washing.In vivo: Imaging experiments were carried out in baboons with an external Dacron shunt between the femoral artery and vein. Gamma camera images following 123I-anti-PADGEM infusion (1.0 mCi; 300 μg) demonstrated intense uptake in the thrombus induced by the Dacron vascular graft within 10 minutes. The graft:blood pool activity ratio was 33:1. Control experiments with 123I-nonimmune IgG showed minimal uptake. 123I-anti-PADGEM cleared the circulating blood pool with an initial half-disappearance time of 2-6 minutes. The primary routes of metabolism were hepatic uptake, dehalogenation and urinary excretion of free iodine. There was no evidence that the anti-PADGEM antibodies had any adverse effects on the normal processes of hemostasis in any of these experiments.Anti-PADGEM antibodies, both monoclonal and polyclonal, are directed against activated platelets in thrombi or in areas of tissue injury; they do not bind to resting platelets in the circulation. Radioimmunoscintigraphy with these agents provides a novel approach to the noninvasive detection and localization of thrombi in vivo, with potential application to human disease. Furthermore, linkage of these antibodies to fibrinolytic enzymes offers a strategy for the specific lysis of thrombi in vivo.