Academic literature on the topic 'B lymphocyte'

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Journal articles on the topic "B lymphocyte"

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Tait, Heidi. "Mechanisms behind the induction of Ttc7 transcription during B lymphocyte development(93.35)." Journal of Immunology 184, no. 1_Supplement (April 1, 2010): 93.35. http://dx.doi.org/10.4049/jimmunol.184.supp.93.35.

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Abstract Changes in Ttc7 (tetratricopeptide repeat domain 7) transcription have been associated with changes in B lymphocyte signaling through changes in both the lymphopoietic environment and homeostasis of B lymphocyte development in mice with the Ttc7fsn/fsn(flaky skin) mutation. We have demonstrated that young Ttc7fsn/fsn mice exhibit decreased naive B lymphocyte populations in the bone marrow and spleen as compared to their wild type littermates, and that this disparity is exaggerated with age. The Ttc7fsn/fsn mutation also leads to excessive production of harmful B1b lymphocytes causing autoimmune disease closely related to SLE. This is significant as both autoimmune and aging human populations share similar B lymphocyte profiles. The evaluation of signaling events upstream of Ttc7 transcription will shed light on stage-specific B cell developmental signaling mechanisms in the bone marrow and spleen that cause immunological dysfunction. We have begun to classify B lymphocyte stages at which Ttc7 transcription rates fluctuate in pursuit of these signaling mechanisms. We have found Ttc7 to be transcribed in the bone marrow at early B lymphocyte stages and have evidence that its transcription is repressed at later stages in the spleen. To further support the hypothesis that induction of Ttc7 transcription during B cell development occurs in early B lymphocytes, we have also found that a 1kb segment of the promoter induces a higher rate of transcription in the pre-B 70Z/3 cell line.
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M, Leclerc. "The Sea Star B Lymphocyte." Vaccines & Vaccination Open Access 8, no. 2 (August 4, 2023): 1–2. http://dx.doi.org/10.23880/vvoa-16000163.

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Milicevic, Novica. "T lymphocytes are necessary for the peripheral phase of B lymphocyte maturation." Srpski arhiv za celokupno lekarstvo 136, Suppl. 2 (2008): 166–70. http://dx.doi.org/10.2298/sarh08s2166m.

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Until recently, B lymphocyte maturation was considered to be independent of the thymus and T lymphocytes. However, using nude animals, which lack the functional thymus, we have shown that T lymphocytes are required for the peripheral phase of B lymphocyte maturation. We showed that the proportion of immature B lymphocyte subsets (CD90highIgMhigh and CD90highIgMlow) was significantly increased, whereas that of mature B lymphocyte subsets (CD90?IgMlow and CD90?IgMhigh) was decreased in the peripheral blood and lymph nodes of nude rats. In addition, the expression of functionally important surface molecules MHC class II, ICAM-1, CD44 and L-selectin was significantly down-regulated both on immature and mature B lymphocyte subsets. The implantation of thymic tissue under the kidney capsule of nude rats alleviated the block in B lymphocyte maturation and normalized of the defective expression of surface molecules. Comparable effects were seen after the adoptive transfer of T lymphocytes. This shows that in nude rats B lymphocytes do not mature properly due to the lack of T cell help and that T lymphocytes are required for the peripheral phase of B lymphocyte maturation, as well as for the appropriate expression of surface molecules. This should be considered when treating patients with T lymphocyte deficiencies.
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Silber, R., CM Farber, E. Papadopoulos, D. Nevrla, L. Liebes, M. Bruck, R. Brown, and ZN Canellakis. "Glutathione depletion in chronic lymphocytic leukemia B lymphocytes." Blood 80, no. 8 (October 15, 1992): 2038–43. http://dx.doi.org/10.1182/blood.v80.8.2038.2038.

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Abstract Glutathione (GSH) content may be the major determinant of a cell's sensitivity to cytotoxic alkylating agents. In the present study, the GSH concentration was determined in lymphocytes isolated from the blood of normal subjects and patients with chronic lymphocytic leukemia (CLL). Comparable levels were found in both types of cells. Incubation for 20 hours led to a decrease in GSH to 51% of baseline values in CLL B cells. Under the same conditions, normal B- or T-lymphocyte GSH content remained constant. GSH depletion was shown to be a characteristic of the B-CLL B lymphocyte. It was not found in the T cells of patients with B-CLL or in cells from patients with T-CLL. Chlorambucil (CLB) contributes to the decrease in GSH in B-CLL lymphocytes; after incubation with the drug, lower levels of GSH were found than in the normal B or T lymphocytes, B-CLL T cells, or T-CLL (CD4 or CD8) cells. GSH depletion of CLL B lymphocytes may be related to the greater therapeutic efficacy of CLB in B-CLL than in T-CLL.
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Silber, R., CM Farber, E. Papadopoulos, D. Nevrla, L. Liebes, M. Bruck, R. Brown, and ZN Canellakis. "Glutathione depletion in chronic lymphocytic leukemia B lymphocytes." Blood 80, no. 8 (October 15, 1992): 2038–43. http://dx.doi.org/10.1182/blood.v80.8.2038.bloodjournal8082038.

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Glutathione (GSH) content may be the major determinant of a cell's sensitivity to cytotoxic alkylating agents. In the present study, the GSH concentration was determined in lymphocytes isolated from the blood of normal subjects and patients with chronic lymphocytic leukemia (CLL). Comparable levels were found in both types of cells. Incubation for 20 hours led to a decrease in GSH to 51% of baseline values in CLL B cells. Under the same conditions, normal B- or T-lymphocyte GSH content remained constant. GSH depletion was shown to be a characteristic of the B-CLL B lymphocyte. It was not found in the T cells of patients with B-CLL or in cells from patients with T-CLL. Chlorambucil (CLB) contributes to the decrease in GSH in B-CLL lymphocytes; after incubation with the drug, lower levels of GSH were found than in the normal B or T lymphocytes, B-CLL T cells, or T-CLL (CD4 or CD8) cells. GSH depletion of CLL B lymphocytes may be related to the greater therapeutic efficacy of CLB in B-CLL than in T-CLL.
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Winther, Birgit, Donald J. Innes, John Bratsch, and Frederick G. Hayden. "Lymphocyte Subsets in the Nasal Mucosa and Peripheral Blood during Experimental Rhinovirus Infection." American Journal of Rhinology 6, no. 4 (July 1992): 149–56. http://dx.doi.org/10.2500/105065892781874621.

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The local cellular response during rhinovirus infection was studied with immunohistochemical staining of lymphocyte subpopulations in the lamina propria of the nasal mucosa (inferior turbinate) in 25 biopsies from volunteers with experimental rhinovirus colds and compared with biopsies from healthy volunteers. Biopsies from rhinovirus infected volunteers, taken either in the early phase of the infection (days 3 and 5) or during convalescence (day 14) were evaluated in a semiquantitative fashion for degree of infiltration. Lymphocyte subpopulations also were counted on coded specimens. During experimental rhinovirus infection, no change could be observed in the overall degree of lymphocytic infiltration or in the numbers of T and B lymphocytes compared with control specimens. The overall degree of lymphocyte infiltration in the nasal mucosa was mild to moderate and consisted principally of T lymphocytes and only a few scattered B lymphocytes. Few natural killer lymphocytes were seen. These findings are similar to those in normal nasal mucosa and in contrast to the findings after topical application of recombinant interferon, which often results in a heavy lymphocyte infiltration. Lymphocyte subpopulation in the peripheral blood did not change when compared with prechallenge values in nine rhinovirus-infected volunteers.
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Li, Jianxu, Peng Guo, Masayuki Hirano, Brantley Herrin, and Max Cooper. "Cellular and molecular characterization of hagfish VLR-based adaptive immune system (VET2P.1043)." Journal of Immunology 192, no. 1_Supplement (May 1, 2014): 207.15. http://dx.doi.org/10.4049/jimmunol.192.supp.207.15.

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Abstract Jawless vertebrates have an alternative adaptive immune system in which variable lymphocyte receptors (VLR) are somatically diversified through recombinatorial assembly of leucine-rich repeat cassettes during lymphocyte development. Three VLR loci (VLRA, VLRB, and VLRC) have been defined in lampreys and each is expressed by a distinct lymphocyte population. Lamprey VLRA and VLRC are expressed by T-like lineages of lymphocytes, whereas VLRB is expressed by a B-like lineage of lymphocytes, much like αβ T, γδ T and B cells in jawed vertebrates. Recently we have revised the nomenclature for the hagfish VLRs by defining a third VLR gene. Here, monoclonal and polyclonal antibodies were generated against invariant residues of hagfish VLRA, VLRB and VLRC and these were used to identify VLR-bearing lymphocytes and their products. We found that hagfish VLRA, VLRB and VLRC are expressed by three separate lymphocyte populations. Size-exclusion chromatography and western blot analysis indicated that multivalent VLRB proteins are released into the circulation, which suggests that hagfish VLRB+ cells are B-cell like. In contrast, neither VLRA nor VLRC was detectable in the plasma, supporting the hypothesis that these two lymphocyte populations are T-cell like. The demonstration of three lymphocyte populations in both lampreys and hagfish suggests that this tripartite lymphocytic differentiation program already existed in a common ancestor of the two cyclostome lineages around 480 Mya.
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HASEGAWA, Minoru. "B lymphocyte." Japanese Journal of Clinical Immunology 28, no. 5 (2005): 300–308. http://dx.doi.org/10.2177/jsci.28.300.

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Dorward, D. "Interactions Between Mouse Lymphocytes And Borrelia Burgdorferi, The Infectious Agent Of Lyme Disease." Microscopy and Microanalysis 5, S2 (August 1999): 1242–43. http://dx.doi.org/10.1017/s143192760001953x.

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Lyme disease is a tick borne, multi-system disorder caused by low density systemic infections with the spirochete Borrelia burgdorferi. Without antimicrobial treatment, mammalian infections with these bacteria are persistent and chronic. Recent studies showed that B. burgdorferi can target, invade, and lyse both cultured and primary human B and T cells. Direct interactions between the spirochetes and lymphocytes also leads to adherence of B and T cell antigens on the surface of significant proportions of the bacteria . Adherent lymphocytic antigens inhibit binding of antibodies to prominent B. burgdorferi proteins, and interfere with classic complement-mediated killing, suggesting a possible role for spirochete-lymphocyte interactions in immune evasion.In order to develop an experimental animal model for assessing spirochete-lymphocyte interactions, B. burgdorferi and primary mouse lymphocytes were co-incubated and examined by electron microscopy. Mononuclear cells were separated from fresh mouse blood by Ficoll gradient centrifugation (ICN, Biomedicals, Aurora, Ohio).
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Wang, Hui, Li Hong, Yangyang Tang, Meizhen Xu, Shuai Pan, Qingling Wang, and Cheng He. "Generation of a B-1 lymphocyte-specific conditional knockout mouse model Bhlhe41tdTomato-Cre." Journal of Immunology 202, no. 1_Supplement (May 1, 2019): 130.40. http://dx.doi.org/10.4049/jimmunol.202.supp.130.40.

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Abstract B-1 lymphocytes play indispensable roles in defensing a wide range of pathogens prior to adaptive immune response arising. Although several transgenic mouse models targeting different stages of B lymphocytes have been established e.g. Cd19-Cre and Mb1-Cre, a B-1 lymphocyte specific conditional knockout mouse model for illuminating the role of a gene of interest in B-1 lymphocytes is still missing. In this study, we aimed to generate a B-1 lymphocyte-specific knockout mouse model by expression of Cre recombinase under the control of the promoter of Bhlhe41, which is preferentially expressed in B-1 lymphocyte and microglia in immune system. A tdTomato-2A-Cre-polyA cassette was inserted to the locus of Bhlhe41 by CRISPR-CAS9 technology. Bhlhe41tdTomato-Cre/+Rosa26EYFP/+ mice were generated for determining Cre-mediated recombination efficiency. The accuracy of insertion of tdTomato-2A-Cre-polyA cassette to Bhlhe41 locus was confirmed by significantly reduced peritoneal B-1a lymphocytes in Bhlhe41tdTomato-Cre/tdTomato-Cre mice. Flow cytometric analysis of tdTomato in immune cells from Bhlhe41tdTomato-Cre/+confirmed the specific expression of BHLHE41 in B-1 lymphocytes rather than other B subsets. Further analysis of EYFP in immune cells from Bhlhe41tdTomato-Cre/+Rosa26EYFP/+ mice revealed larger than 90% recombination in splenic and peritoneal B-1 lymphocytes while less than 10% recombination in other B subsets. Hence, we generated a B-1 lymphocyte-specific conditional knockout mouse model Bhlhe41tdTomato-Cre, which can be used for studying the function of a specific gene in B-1 lymphocyte-mediated immune responses.
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Dissertations / Theses on the topic "B lymphocyte"

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Greenwood, M. R. "B lymphocyte differentiation." Thesis, Imperial College London, 1986. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.375109.

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Bonnefoy-Berard, Nathalie. "Induction et régulation de l'activation des lymphocytes T et B par les globulines antilymphocytaires." Lyon 1, 1992. http://www.theses.fr/1992LYO1H086.

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Obino, Dorian. "Molecular mechanisms regulating B lymphocyte polarization." Thesis, Sorbonne Paris Cité, 2016. http://www.theses.fr/2016USPCB031/document.

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Dans les organes lymphoïdes secondaires, les lymphocytes B acquièrent des antigènes immobilisés à la surface de cellules voisines. L’engagement du BCR (récepteur des cellules B) avec de tels antigènes induit la formation d’une synapse immunologique et la polarisation des lymphocytes B. Cette polarisation inclut le repositionnement du centrosome à la synapse immunologique ainsi que le recrutement et la sécrétion locale des lysosomes qui sont nécessaires à l’extraction, l’apprêtement et la présentation des antigènes sur les molécules du complexe majeur d’histocomptabilité de classe II (CMH-II) aux lymphocytes T CD4+ pré-activés. Des travaux précurseurs menés dans le laboratoire ont permis de mettre en évidence les premiers acteurs moléculaires impliqués dans ce processus. Cependant, le mécanisme précis gouvernant la polarisation du centrosome demeure encore aujourd’hui inconnu. Le travail réalisé pendant cette thèse avait pour objectif d’identifier de nouveaux régulateurs contrôlant la polarisation du centrosome dans les lymphocytes B après engagement du BCR avec des antigènes immobilisés. De plus, au regard du rôle grandissant joué par le microenvironnement tissulaire dans l’activation des lymphocytes B ainsi que dans la modulation de leurs fonctions, nous avons étudié l’effet de la protéine extracellulaire Galectine-8 sur la régulation de la capacité des lymphocytes B à se polariser et à extraire et présenter des antigènes immobilisés. Le travail présenté dans ce manuscrit montre que la présence du complexe Arp2/3 au centrosome des lymphocytes B non activés permet la nucléation locale de filaments d’actine qui permettent, grâce à leur interaction avec le complexe LINC, de lier le centrosome au noyau. L’activation des lymphocytes B induit la déplétion partielle du complexe Arp2/3 du centrosome qui est recruté à la synapse immunologique par la protéine HS1. Ceci induit une diminution de la nucléation d’actine au centrosome entraînant la séparation entre le centrosome et le noyau et permettant la polarisation du centrosome vers la synapse. De plus, nous montrons que la présence de la protéine Galectine-8 dans le milieu extracellulaire favorise le recrutement et la sécrétion des lysosomes à la synapse immunologique, conférant aux lymphocytes B une meilleure capacité à extraire et présenter des antigènes immobilisés. Nos résultats mettent en évidence des mécanismes inattendus régulant la polarisation des lymphocytes B en réponse à une stimulation antigénique et soulèvent des questions intéressantes concernant la régulation coordonnée de ces mécanismes qui confèrent aux lymphocytes B la capacité d’extraire, d’apprêter et de présenter des antigènes immobilisés efficacement
In secondary lymphoid organs, B cells acquire antigens that are tethered at the surface of neighboring cells. Engagement of the B cell receptor (BCR) with such immobilized antigens leads to the formation of an immune synapse and the subsequent polarization of B cells. This includes the repositioning of the centrosome towards the immune synapse as well as the recruitment and local secretion of lysosomes required for efficient antigen extraction, processing and presentation onto class II major histocompatibility complex (MHC-II) molecules to primed CD4+ T cells. Pioneer work performed in the lab has highlighted the first molecular players involved in this process. However, the precise mechanism governing centrosome polarization remains to be fully elucidated. The work performed during this thesis aimed at identifying new regulators supporting centrosome polarization in B lymphocytes upon BCR engagement with immobilized antigens. In addition, in view of the emerging role played by the tissue microenvironment in shaping B cell activation and functions we investigated whether extracellular Galectin-8 modulates the ability of B cells to polarize, extract and present immobilized antigens. We show here that, in resting lymphocytes, centrosome-associated Arp2/3 (actin related protein-2/3) locally nucleates F-actin, which is needed for centrosome tethering to the nucleus via the LINC (linker of nucleoskeleton and cytoskeleton) complex. Upon lymphocyte activation, Arp2/3 is partially depleted from the centrosome as a result of its HS1-dependent recruitment to the immune synapse. This leads to a reduction in F-actin nucleation at the centrosome and thereby allows its detachment from the nucleus and polarization to the synapse. In addition, we show that extracellular Galectin-8 favors lysosome recruitment and secretion at the immune synapse, hence providing B cells with an enhanced capacity to extract and present immobilized antigens. Our findings highlight unexpected mechanisms that tune B cell polarity in response to antigenic stimulation and raise exciting questions concerning the coordinated regulation of these mechanisms to provide B cells with the capacity to efficiently extract, process and present surface-tethered antigens
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Bonnefoix, Thierry. "Les lymphocytes T intra-tumoraux dans les lymphomes malins non hodgkiniens B : activation, prolifération et production de facteurs de régulation des cellules B." Grenoble 1, 1991. http://www.theses.fr/1991GRE10153.

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Les lymphocytes t sont constamment presents dans les ganglions envahis par un lymphome malin non hodgkinien b. Ce travail a permis de reunir des arguments en faveur de l'implication de ces cellules t dans le processus tumoral: diminution de la capacite des cellules t a produire de l'interleukine 2 (il2) et a proliferer en presence de pha; pourcentages eleves de cellules t dr+ (activees), et cd4+cd45ra-(memoires), ainsi que de cellules t cd25+ (p55 du recepteur de l'il2); a partir des cellules t cd25+ totales, il a ete obtenu des clones t capables de proliferer au contact des cellules b malignes autologues, mais pas au contact des cellules b normales (b-ebv) autologues; la nature des relations fonctionnelles entre les cellules t intra-tumorales et les cellules b malignes autologues reste a determiner: en utilisant des cellules b normales comme cibles des cellules t, il n'a pu etre mis en evidence aucune anomalie de production d'activites bcgf et bcdf mu et gamma
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McCrea, Anthony Philip. "The role of the T lymphocyte in B cell chronic lymphocytic leukaemia." Thesis, Queen's University Belfast, 1989. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.335939.

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Liu, Si. "B lymphocyte function in surgical anergic patients." Thesis, McGill University, 1988. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=64094.

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Akha, Amir Akbar Sadighi. "Signalling through the B lymphocyte antigen receptor." Thesis, University of Oxford, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.318620.

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Kenney, John Stephen. "Functional antibody diversity of B-Lymphocyte hybridomas." Strasbourg 1, 1996. http://www.theses.fr/1996STR12363.

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Lemoine, Sébastien. "Étude du rôle du lymphocyte B dans la tolérance périphérique." Brest, 2011. http://www.theses.fr/2011BRES2308.

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Le système immunitaire est équipé de nombreux points de contrôle pour maintenir la tolérance et prévenir l'autoimmunité. Les mécanismes opérant en périphérie sont principalement médiés par les lymphocytes T régulateurs. Dans le contexte de l’autoimmunité, les lymphocytes B sont généralement considérés pathogéniques car produisant des anticorps pouvant causer des dommages aux tissus ciblés. Cependant leur déplétion dans plusieurs modèles murins de maladies autoimmunes induit une pathologie plus sévère, donnant ainsi aux lymphocytes B un rôle régulateur insoupçonné. Des pistes ont été découvertes chez la souris quant au mécanisme d’action et au phénotype de ces cellules B régulatrices et deux sous populations de lymphocytes B sécrétant de l'interleukine 10 ont été décrites. Cependant malgré un intérêt croissant pour la biologie des lymphocytes B régulateurs, l’existence d’une population équivalente chez l’homme est toujours controversée. Cette étude montre que les lymphocytes T activés peuvent induire leur propre régulation par un mécanisme qui dépend des lymphocytes B. Les lymphocytes B régulateurs identifiés comme CD19high IgD+ CD24high CD38high CD5high, inhibent la prolifération et la sécrétion des cytokines pro-inflammatoires des lymphocytes TH1. Deux mécanismes distincts sont requis. L’inhibition des sécrétions des lymphocytes T fait intervenir l’interleukine 10 sécrétée par les lymphocytes B et l’inhibition de la prolifération des lymphocytes T fait appel à l’induction de lymphocytes T régulateurs. L’évaluation de cette nouvelle fonction régulatrice dans les maladies autoimmunes montre que la régulation médiée par les lymphocytes B est déficiente dans le Lupus Erythémateux Disséminé
Nature has provided the immune system with numerous checkpoints controlling the maintenance of tolerance and the prevention of autoimmunity. The regulatory mechanisms operating in the periphery of the immune system are mediated mainly by a specific population of regulatory T cells considered as the main contributor to peripheral tolerance. In auto immunity, B cells are generally considered pathogenic since they release autoantibodies, that can cause damages to target tissues. However B cell depletion in several murine models of autoimmune diseases leads to a more severe pathology, giving B cells an unexpected regulatory role. Insights have been realized concerning the mechanism of action and the phenotype of this particular subset of regulatory B cells in mice and two subsets of IL-10 secreting B cells have been endowed with regulatory properties. However, despite increasing interest in regulatory B cell biology, the existence of an equivalent population in human is still a matter of controversy. The current study indicates that activated T cells can induce their own regulation by promoting the development of a B-cell dependent regulatory process. Regulatory B cells, identified by their expression of CD19high IgD+ CD24high CD38high CD5high, inhibit the proliferation and cytokine secretion of proinflammatory TH1 cells with the contribution of regulatory T cells, placing B cells at the center of immunosuppressive reactions. The assessment of this new regulatory function in autoimmune diseases shows that B-cell mediated immune regulation is deficient in Systemic Lupus Erythematosus
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Haas, Karen Marie. "Induction and regulation of bovine B lymphocyte responses /." free to MU campus, to others for purchase, 2000. http://wwwlib.umi.com/cr/mo/fullcit?p9999290.

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Books on the topic "B lymphocyte"

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1948-, Cambier John C., ed. B-lymphocyte differentiation. Boca Raton, Fla: CRC Press, 1986.

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Graham, Bird Angus, and Calvert Jane E, eds. B lymphocytes in human disease. Oxford: Oxford University Press, 1988.

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Sudhir, Gupta, ed. Mechanisms of lymphocyte activation and immune regulation XI: B cell biology. New York: Springer, 2007.

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Clemens, Sorg, ed. Molecular biology of B cell developments. Basel: Karger, 1990.

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N, Witte Owen, Klinman Norman, Howard Maureen C, Abbott Laboratories, Ortho Pharmaceutical Corporation, University of California, Los Angeles., and UCLA Symposium on B Cell Development (1988 : Taos, N.M.), eds. B cell development: Proceedings of an Abbott-Ortho-UCLA symposium held at Taos, New Mexico, January 31-February 7, 1988. New York: A.R. Liss, 1988.

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Singh, Harinder, and Rudolf Grosschedl, eds. Molecular Analysis of B Lymphocyte Development and Activation. Berlin/Heidelberg: Springer-Verlag, 2005. http://dx.doi.org/10.1007/b137478.

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Korber, Bette. HIV molecular immunology 2006/2007. Edited by Los Alamos National Laboratory. Theoretical Biology and Biophysics Group T-10. Los Alamos, N.M: Los Alamos National Laboratory, Theoretical Biology and Biophysics Group T-10, 2006.

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1950-, Grinstein Sergio, and Rotstein Ori D, eds. Mechanisms of leukocyte activation. San Diego: Academic Press, 1990.

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Morrow, Maureen A. Developmentally restricted and IL-7 controlled pre-B lymphocyte gene expression. [New York]: Columbia University, 1992.

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Finney, Michael. A study in the molecular basis of human B lymphocyte activation. Birmingham: University of Birmingham, 1991.

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Book chapters on the topic "B lymphocyte"

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Gooch, Jan W. "B Lymphocyte." In Encyclopedic Dictionary of Polymers, 878. New York, NY: Springer New York, 2011. http://dx.doi.org/10.1007/978-1-4419-6247-8_13272.

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Pillai, Shiv. "Antigen-Induced B-Lymphocyte Differentiation." In Lymphocyte Development, 321–72. Boston, MA: Birkhäuser Boston, 2000. http://dx.doi.org/10.1007/978-1-4612-2444-0_8.

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Pillai, Shiv. "The Generation of Naive B Lymphocytes." In Lymphocyte Development, 265–320. Boston, MA: Birkhäuser Boston, 2000. http://dx.doi.org/10.1007/978-1-4612-2444-0_7.

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Kumar, Rashmi. "B Lymphocyte Antigen CD19." In Encyclopedia of Signaling Molecules, 513–22. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-67199-4_101837.

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Kumar, Rashmi. "B Lymphocyte Antigen CD19." In Encyclopedia of Signaling Molecules, 1–10. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4614-6438-9_101837-1.

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Forbes, Ian J., and Anthony S.-Y. Leong. "B Cell Differentiation." In Essential Oncology of the Lymphocyte, 127–41. London: Springer London, 1987. http://dx.doi.org/10.1007/978-1-4471-1467-3_11.

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Forbes, Ian J., and Anthony S.-Y. Leong. "B Cell Activation." In Essential Oncology of the Lymphocyte, 143–60. London: Springer London, 1987. http://dx.doi.org/10.1007/978-1-4471-1467-3_12.

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Forbes, Ian J., and Anthony S.-Y. Leong. "B Cell Neoplasia." In Essential Oncology of the Lymphocyte, 199–207. London: Springer London, 1987. http://dx.doi.org/10.1007/978-1-4471-1467-3_15.

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Forbes, Ian J., and Anthony S.-Y. Leong. "B Cell Leukaemias." In Essential Oncology of the Lymphocyte, 209–42. London: Springer London, 1987. http://dx.doi.org/10.1007/978-1-4471-1467-3_16.

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Forbes, Ian J., and Anthony S.-Y. Leong. "B Cell Lymphomas." In Essential Oncology of the Lymphocyte, 243–87. London: Springer London, 1987. http://dx.doi.org/10.1007/978-1-4471-1467-3_17.

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Conference papers on the topic "B lymphocyte"

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Castellini, Alberto, Giuditta Franco, and Antonio Vella. "Age-related relationships among peripheral B lymphocyte subpopulations." In 2017 IEEE Congress on Evolutionary Computation (CEC). IEEE, 2017. http://dx.doi.org/10.1109/cec.2017.7969528.

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Filippi, J. F., D. Arnoux, N. Tubiana, B. Boutière, F. Le Caär, J. Sampol, Lab Hématol, Pr J. Sampol, and Pr Y. Carcassonne. "PLASMINOGEN ACTIVATOR ACTIVITY OF NORMAL AND MALIGNANT MONONUCLEAR HUMAN CELLS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643167.

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Plasminogen activators (PA) are thought to play a role in the invasive and metastatic properties of many types of cancer cells. Though, discrepancies in correlations between fibrinolytic activity and metastatic potential of malignant cells have been described.In this study, we evaluated both tissue type (tPA) and urokinase type (UK) cellular PA activities in different mononuclear cell types : normal T and B human peripheral lymphocytes, B cells from patients with chronic lymphocytic leukemia (CLL), human blood monocytes, alveolar macrophages, U 937, RAJI and JM cell 1ines.Mononuclear cells were isolated by Ficoll-hypaque gradients and monocytes by plastic adhesion. T and B cells were separated by a rosetting technique using sheep red blood cells. Cellular extracts were prepared by 0.5 % Triton X 100 buffer treatment followed by sonication and centrifugation 10 ' at 2000 g. PA assays were performed on the supernatants.UK-type PA was evaluated by a liquid-phase assay in presence of human plasminogen (Kabi) and chromogenic substrate S 2251 (Kabi).tPA was determinated using a solid-phase fibrin activity assay which involves an affinity separation step and thus allows selective detection of tPA.In both cases, results were reported in international units by reference to standard curves of UK (Choay) or tPA (Kabi).In all cell types tested, PA detected was essentially urokinase-type. Highest PA activity was found in U 937 cells (0.7 IU/5×l06 cells). In normal blood lymphocytes, mean PA activity was 0.08 IU/5×l06 cells. Examination of lymphocytes from patients with CLL revealed a marked decrease in UK activity as compared to normals (< 0.01 IU/5×106 cells in more than 50 % cases).The function of PA in normal lymphocyte physiology and the potential pathogenic role of diminished PA in CLL lymphocytes remains to be investigated.
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Schneider, L., V. Hax, N. Marcondes, RM Xavier, and R. Chakr. "AB0174 Lymphocyte subsets t, b and nk cels in systemic sclerosis." In Annual European Congress of Rheumatology, 14–17 June, 2017. BMJ Publishing Group Ltd and European League Against Rheumatism, 2017. http://dx.doi.org/10.1136/annrheumdis-2017-eular.7028.

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Schneider, L., V. Hax, N. Marcondes, RM Xavier, and R. Chakr. "AB0645 Lymphocyte subsets t, b and nk cells in systemic sclerosis." In Annual European Congress of Rheumatology, 14–17 June, 2017. BMJ Publishing Group Ltd and European League Against Rheumatism, 2017. http://dx.doi.org/10.1136/annrheumdis-2017-eular.7032.

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Aydar, S., S. Alataş, L. Numanoğlu, and A. Sönmezdağ. "EFFECT OF ORAL ANTICOAGULANTS ON STABLE ROSETTE FORMATION." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643271.

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Human peripheral blood T lymphacytes when cultered in the presence of mitogen Phytohemogglutinin (PHA) acquire the capacity to form E rosettes with sheep erythrocytes that are resistant to incubation at 37° C. Whereas human thymus lymphocytes form 37° C stable E rosettes. On the other hand, it is shown that the use of anticoagulants can prevent cancer metastases which brings forth the importance of explaining the relationship between the lymphocyte functions and anticoagulant action mecha-nismus. In order to investigate this relationship, we did a group af experiments with lymphocytes of normal children and of children with severe burn wounds. Peripheral blood lymphocytes were seperated by “Lymphoprep” centrifugation technique. The lymphocytes of normal children and patients with burn were divided in two groups: A-Activated lymphocytes: 1×106 /ml lymphocytes were cultured and activated by PHAfor 48 hours at 37° C in RPMI 1640. B-Non activated lymphocytes were in culture witout PHA. 1×10™6 M/ml warfarin sulfate was added to some of the cultures of each group prior to the culture conditions. At the end of the 48 hour incubation, heat stable rosette formation was determined by the method of Wauve and co-workers. Significantly elevated levels of heat stable rosette forming cells were found in the PHA activated culture treated with warfarin sulfate in normals and patients with burn. Although the blastic transformation of T lymphocytes was found to be depressed, heat stable rosette formation of warfarin sulfate treated lymphocytes abtained from burn patients was observed to be significantly elevated. It is concluded that warfarin sulfate increases the activity of T lymphocytes by interfering with the resynthesis of heai stable E receptors.
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Qian, Meilin, Fei Ye, Chen Zhang, Jianming Wang, Yuanli Zhang, Yangyang Cui, Linli Li, Xiaoli Gou, and Jia Ni. "Abstract 3761: HSK26784: An oral PROTAC-BTK degrader for multiple B lymphocyte derived malignancies." In Proceedings: AACR Annual Meeting 2020; April 27-28, 2020 and June 22-24, 2020; Philadelphia, PA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.am2020-3761.

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Salgado, Amanda Forte Mendes Tejo, Maria Eduarda Borges Kerstenetzky, Vitoria Ferreira David Melquiades, Marcelo Ramos Tejo Salgado, and Leuridan Cavalcante Torres. "ANALYSIS OF CD80- AND CD86-EXPRESSING B-LYMPHOCYTE LEVELS IN THE BLOOD OF WOMEN WITH LOCALLY ADVANCED TRIPLENEGATIVE BREAST CANCER." In Abstracts from the Brazilian Breast Cancer Symposium - BBCS 2021. Mastology, 2021. http://dx.doi.org/10.29289/259453942021v31s2021.

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Objective: To assess the levels of CD80 and CD86-expressing B lymphocytes in the blood of women with locally advanced triple-negative breast cancer (TNBC). Methods: This is a prospective and exploratory cohort study involving 30 women with TNBC and 30 healthy controls, conducted in 2018–2019. Peripheral blood collection was performed prior to chemotherapy. Immunophenotyping of B lymphocytes and CD80 and CD86 molecules was performed by flow cytometry. Women were evaluated for the degree of pathological response to chemotherapy and divided into groups with full (RC) or partial (RP) pathological response. Nonparametric Mann–Whitney U-test was used for comparison between two groups. Values of p<0.05 were considered statistically significant. Analyses were performed using Graphpad v7.0 software. Results: We analyzed 30 patients with locally advanced TNBC. The age of the patients ranged from 27 to 59 years, and median age was 44.5 years (35.5–51.7). Regarding menopausal status, 62.1% were premenopausal and 37.9% postmenopausal. Regarding the nuclear grade, 63% of the tumors were grade 3, followed by 27% grade 2. In relation to the clinical stage, 30% were in stage IIIA, 63.4% stage IIIB, and 6.6% stage IIIC. In the evaluation of response to neoadjuvant treatment, 56.7% of patients had complete pathological response, and 43.3% had partial response. TNBC patients had high levels of CD86 + B lymphocytes when compared with controls (p <0.0001). Regarding total B and CD80 + B levels—no significant differences were observed between the groups. In the analysis of CD86 and CD80 expression and total B cell levels, no significant differences were observed between the RC and RP groups. Conclusion: This study showed that the immune system of patients with TNBC can regulate costimulatory molecules in circulating B cells, probably in response to the disease.
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Salgado, Amanda Forte Mendes Tejo. "ANALYSIS OF CD80 AND CD86-EXPRESSING B LYMPHOCYTE LEVELS IN THE BLOOD OF WOMEN WITH LOCALLY ADVANCED TRIPLE NEGATIVE BREAST CANCER." In Scientifc papers of XXIII Brazilian Breast Congress - 2021. Mastology, 2021. http://dx.doi.org/10.29289/259453942021v31s1053.

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Introduction: Breast Cancer was the second most common malignant neoplasm and the leading cause of cancer-related deaths in women worldwide in 2018; it can be classified according to the immunohistochemical pattern in four main tumor subtypes, with triple negative breast cancer (TNBC) being the most aggressive subtype with the worst prognosis, representing a public health problem. With the advancement of knowledge about the biology of tumors, the importance of understanding the interactions between the tumor, the tumor microenvironment and immune system cells has come to light, especially the role of CD80 and CD86 co-stimulator molecules in the activation of TCD4+ lymphocytes, cytokine production and proliferation of these cells against tumor antigens. Objectives: To assess the levels of CD80 and CD86-expressing B lymphocytes in the blood of women with locally advanced triple negative breast cancer. Methods: This is a prospective and exploratory cohort study of 30 women with triple negative breast cancer and 30 healthy controls, conducted in 2018– 2019. Peripheral blood collection was performed prior to chemotherapy. Immunophenotyping of B lymphocytes and CD80 and CD86 molecules was performed by flow cytometry. Women were evaluated for the degree of pathological response to chemotherapy, and were divided into groups with full (RC) or partial (RP) pathological response. Nonparametric MannWhitney tests were used for comparison between the two groups. Values of p <0.05 were considered significant. Analyzes were performed using Graphpad v7.0 software. Results: We analyzed 30 patients with locally advanced triple-negative breast cancer. The age of the patients ranged from 27 to 59 years, median age was 44.5 years (35.5–51.7), most patients were in the age group ≤50 years (43.3%). Regarding menopausal status, 62.1% were premenopausal and 37.9% postmenopausal. Regarding the nuclear grade, 63% of the tumors were grade 3, followed by 27% grade 2. In relation to clinical stage, 30% were in stage IIIA, 63.4% stage IIIB and 6.6% stage IIIC. In the evaluation of response to neoadjuvant treatment, 56.7% of patients had complete pathological response, and 43.3% partial response. TNBC patients had high levels of CD86 + B lymphocytes when compared to controls (p <0.0001). Regarding total B and CD80 + B levels - no significant differences were observed between the groups. In the analysis of CD86 and CD80 expression and total B cell levels, no significant differences were observed between the RC and RP groups. Conclusions: This study showed that the immune system of patients with triple negative breast cancer is able to regulate costimulatory molecules in circulating B.
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Teng, Chiao-Fang, Woei-Cherng Shyu, and Long-Bin Jeng. "Abstract 3120: Tumor-infiltrating lymphocyte profiling in hepatitis B virus pre-S2 mutant-positive hepatocellular carcinoma." In Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-3120.

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Kerstenetzky, Maria Eduarda Borges, Amanda Forte Mendes Tejo Salgado, Vitoria Ferreira David Melquiades, Vinicius Rafael Agostinho Gomes, Denise Sobral Viana, Jurema Telles de Oliveira Lima, Marcelo Ramos Tejo Salgado, and Leuridan Cavalcante Torres. "ANALYSIS OF THE LEVEL OF CIRCULATING LEUKOCYTE PLATELET AGGREGATES IN WOMEN WITH BREAST CANCER." In Abstracts from the Brazilian Breast Cancer Symposium - BBCS 2021. Mastology, 2021. http://dx.doi.org/10.29289/259453942021v31s2024.

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Objective: To evaluate the levels of circulating platelet–leukocyte aggregates in women with breast cancer (BC). Methods: A cross-sectional study was carried out between 2018 and 2019 with 27 women, who aged between 18 and 60 years, diagnosed with BC and 15 healthy women (controls). For the evaluation of the circulating platelet aggregate, samples of peripheral blood were collected at the time of routine laboratory tests for diagnosis and before treatment. Platelet aggregate analysis was performed using monoclonal antibodies by flow cytometry. Mann–Whitney U and Kruskal–Wallis tests were used to analyze medians between two and three groups, respectively. Values of p<0.05 were considered statistically significant. Analyses were performed on Graphpad v7.0. Results: In the analysis of the percentages of platelet–lymphocyte aggregates (AGP – lymphocytes) and platelet–neutrophils (AGP – neutrophils), no significant differences were observed between patients and controls. However, it was observed that the patients presented high percentage values of aggregate platelet–monocytes (AGP–monocytes) when compared with controls (p<0.0001). No significant differences were observed in the percentage levels of AGP–lymphocytes and AGP–neutrophils between the luminous subtypes A/B, HER2+, and triple-negative, and between these tumor subtypes and controls. The percentage values of AGP – monocytes were high in the luminous subtypes A/B, HER2+, and triple negative when compared with controls (p=0.008, 0.0001, 0.0002, respectively). However, no significant percentage differences in AGP–monocytes were observed between tumor subtypes. Conclusion: The present study showed the involvement of AGP–monocyte in triple-negative breast cancer and HER2+, these tumor subtypes being more aggressive and with a worse prognosis. Based on these data, the importance of new studies based on an investigation of the role of interactions between platelets and immune system cells in breast cancer became clear. The molecules involved in the linkages between platelets and leukocytes may be possible therapeutic targets.
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Reports on the topic "B lymphocyte"

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Banai, Menachem, and Gary Splitter. Molecular Characterization and Function of Brucella Immunodominant Proteins. United States Department of Agriculture, July 1993. http://dx.doi.org/10.32747/1993.7568100.bard.

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The BARD project was a continuation of a previous BARD funded research project. It was aimed at characterization of the 12kDa immunodominant protein and subsequently the cloning and expression of the gene in E. coli. Additional immunodominant proteins were sought among genomic B. abortus expression library clones using T-lymphocyte proliferation assay as a screening method. The 12kDa protein was identified as the L7/L12 ribosomal protein demonstrating in the first time the role a structural protein may play in the development of the host's immunity against the organism. The gene was cloned from B. abortus (USA) and B. melitensis (Israel) showing identity of the oligonucleotide sequence between the two species. Further subcloning allowed expression of the protein in E. coli. While the native protein was shown to have DTH antigenicity its recombinant analog lacked this activity. In contrast the two proteins elicited lymphocyte proliferation in experimental murine brucellosis. CD4+ cells of the Th1 subset predominantly responded to this protein demonstrating the development of protective immunity (g-IFN, and IL-2) in the host. Similar results were obtained with bovine Brucella primed lymphocytes. UvrA, GroE1 and GroEs were additional Brucella immunodominant proteins that demonstrated MHC class II antigenicity. The role cytotoxic cells are playing in the clearance of brucella cells was shown using knock out mice defective either in their CD4+ or CD8+ cells. CD4+ defective mice were able to clear brucella as fast as did normal mice. In contrast mice which were defective in their CD8+ cells could not clear the organisms effectively proving the importance of this subtype cell line in development of protective immunity. The understanding of the host's immune response and the expansion of the panel of Brucella immunodominant proteins opened new avenues in vaccine design. It is now feasible to selectively use immunodominant proteins either as subunit vaccine to fortify immunity of older animals or as diagnostic reagents for the serological survaillance.
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Su, Bing. The Role of mTOR Signaling in the Regulation of RAG Expression and Genomic Stability during B Lymphocyte Development. Fort Belvoir, VA: Defense Technical Information Center, May 2013. http://dx.doi.org/10.21236/ada588301.

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Liu, Xianqiang, WX Ye, H. Fu, SR Zhu, W. Fu, Yinshuo Han, and Qin Wang. Potential link of neutrophil to lymphocyte ratio with pathological liver conditions in chronic hepatitis B patients: a meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, May 2021. http://dx.doi.org/10.37766/inplasy2021.5.0020.

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Xie, Ping. Regulation of Mitochondria Function by TRAF3 in B Lymphocytes and B Cell Malignancies. Fort Belvoir, VA: Defense Technical Information Center, August 2014. http://dx.doi.org/10.21236/ada610687.

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McElwain, Terry, Eugene Pipano, Guy Palmer, Varda Shkap, Stephen Hines, and Douglas Jasmer. Protection of Cattle Against Babesiosis: Immunization with Recombinant DNA Derived Apical Complex Antigens of Babesia bovis. United States Department of Agriculture, June 1995. http://dx.doi.org/10.32747/1995.7612835.bard.

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Bovine babesiosis caused by Babesia bovis continues to be a significant deterrent to global livestock production. Current control methods have both biological and technical drawbacks that have stimulated research on improved methods of vaccination. This BARD project has focused on characterization of candidate Babesia bovis vaccine antigens located in the apical complex, a unique group of subcellular organelles - including rhoptries, micronemes, and spherical bodies - involved in the invation of erythrocytes. Spherical bodies and rhoptries were partially purified and their contents characterized using monoclonal antibodies. Existing and newly developed monoclonal antibodies bound to antigens in the spherical body, rhoptry, merozoite membrane, and infected erythrocyte membrane. In an initial immunization study using biologically cloned strains, it was demonstrated that strain-common epitopes are important for inducing immune protection against heterologous challenge. Rhoptry-associated antigen 1 (RAP-1) had been demonstrated previously to induce partial immune protection, fulfilled criteria of broad interstrain B and T cell epitope conservation, and thus was further characterized. The RAP-1 gene family consists of at least two gene copies, is homologous to the RAP-1 gene family in B. bigemina, and contains significant sequence similarity to other erythroparasitic protozoan candidate vaccine antigens, including the apical membrane antigen of Plasmodium falciparum. A new RAP-1 monoclonal antibody was developed that inhibits merozoite growth in vitro, demonstrating the presence of a RAP-1 neutralization sensitive domain. Based on these observations, cattle were immunized with Mo7 (Mexico) strain recombinant RAP-1 representing one of the two gene copies. All cattle responded with variable levels of serum antibodies inhibitory to heterologous Israel strain merozoite growth in vitro, and RAP-1 specific T lymphocytes that proliferated when stimulated with either homologous or heterologous native parasite antigen. Minimal protection from clinical disease was present after virulent Israel (heterologous) strain B. bovis challenge. In total, the results support the continued development of RAP-1 as a vaccine antigen, but indicate that additional information about the native structure and function of both RAP-1 gene copies, including the relationship of conserved and polymorphic sequences to B and T cell lepitopes relevant for protection, is necessary for optimization of RAP-1 as a vaccine component.
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Davidson, Irit, Hsing-Jien Kung, and Richard L. Witter. Molecular Interactions between Herpes and Retroviruses in Dually Infected Chickens and Turkeys. United States Department of Agriculture, January 2002. http://dx.doi.org/10.32747/2002.7575275.bard.

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Tumors in commercial poultry are caused mainly by infection with avian herpes and retroviruses, the herpesvirus Marek's disease virus (MDV) and the retroviruses, reticuloendotheliosis (REV), lymphoid leukosis, subgroups A-I and J (ALV and ALV-J) in chickens, or Iymphoprolipherative disease (LPDV) in turkeys. Infection with one virus aggravates the clinical outcome of birds that are already infected by another oncogenic virus. As these viruses do not interfere for infection, MDV and one or more retroviruses can infect the same flock, the same bird and the same cell. While infecting the same cell, herpes and retroviruses might interact in at least three ways: a) Integration of retrovirus genomes, or genomic fragments (mainly the LTR) into MDV;b) alteration of LTR-driven expression of retroviral genes by MDV immediate- early genes, and c) by herpesvirus induced cellular transcriptional factors. The first type of molecular interaction have been demonstrated to happen efficiently in vitro by Dr. Kung, in cases multiple infection of cell cultures with MDV and REV or MDV and ALV. Moreover, Dr. Witter showed that an in vitro-created recombinant, RM1, had altered in vitro replication and in vivo biological properties. A more comprehensive characterization of RM1 was carried out in the present project. We sought to highlight whether events of such integrations occur also in the bird, in vivo. For that, we had first to determine the prevalence of dually-infected individual birds in commercial flocks, as no systematic survey has been yet reported. Surprisingly, about 25% of the commercial flocks infected with avian oncogenic viruses had a multiple virus infection and 5% of the total samples ana lysed had multiple virus sequences. Then, we aimed to evaluate and characterize biologically and molecularly the resulting recombinants, if formed, and to analyse the factors that affect these events (virus strains, type and age of birds and time interval between the infection with both viruses). The perception of retrovirus insertions into herpesviruses in vivo is not banal, as the in vivo and in vitro systems differ in the viral-target cells, lymphocytes or fibroblasts, in the MDV-replicative type, transforming or productive, and the immune system presence. We realized that previous methods employed to study in vitro created recombinant viruses were not adequate for the study of samples taken directly from the bird. Therefore, the Hot Spot-combined PCR was developed based on the molecularly known RM1 virus. Also, the PFGE that was used for tissue cultured-MDV separation was inefficient for separating MDV from organs, but useful with feather tips as a source of bird original MDV. Much attention was dedicated now to feathers, because if a recombinant virus would be formed in vivo, its biological significance would be evident by horizontal dissemination through the feathers. Major findings were: a) not only in vitro, but also in vivo MDV and retrovirus co-infections lead to LTR integrations into MDV. That was shown by the detection of chimeric molecules. These appeared in low quantities and as quasispecies, thus interfering with sequence analysis of cloned gel-purified chimeric molecules. Mainly inserts were located in the repeat long MDV fragments. In field birds chimeric molecules were detected at a lower frequency (2.5%) than in experimentally infected birds (30-50%). These could be transmitted experimentally to another birds by inoculation with chimeric molecules containing blood. Several types of chimeric molecules were formed, and same types were detected in birds infected by a second round. To reproduce viral integrations, in vivo infection trials were done with field inoculate that contained both viruses, but the chimeric molecule yield was undetectable.
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Schat, Karel Antoni, Irit Davidson, and Dan Heller. Chicken infectious anemia virus: immunosuppression, transmission and impact on other diseases. United States Department of Agriculture, 2008. http://dx.doi.org/10.32747/2008.7695591.bard.

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1. Original Objectives. The original broad objectives of the grant were to determine A) the impact of CAV on the generation of cytotoxic T lymphocytes (CTL) to reticuloendotheliosis virus (REV) (CU), B). the interactions between chicken anemia virus (CAV) and Marek’s disease virus (MDV) with an emphasis on horizontal spread of CAV through feathers (KVI), and C) the impact of CAV infection on Salmonella typhimurium (STM) (HUJI). During the third year and the one year no cost extension the CU group included some work on the development of an antigen-antibody complex vaccine for CAV, which was partially funded by the US Poultry and Egg Association. 2. Background to the topic. CAV is a major pathogen causing clinical disease if maternal antibody-free chickens are infected vertically or horizontally between 1 and 14 days of age. Infection after 3 weeks of age when maternal antibodies are not longer present can cause severe subclinical immunosuppression affecting CTL and cytokine expression. The subclinical immunosuppression can aggravate many diseases including Marek’s disease (MD) and several bacterial infections. 3. Major conclusions and achievements. The overall project contributed in the following ways to the knowledge about CAV infection in poultry. As expected CAV infections occur frequently in Israel causing problems to the industry. To control subclinical infections vaccination may be needed and our work indicates that the development of an antigen-antibody complex vaccine is feasible. It was previously known that CAV can spread vertically and horizontally, but the exact routes of the latter had not been confirmed. Our results clearly show that CAV can be shed into the environment through feathers. A potential interaction between CAV and MD virus (MDV) in the feathers was noted which may interfere with MDV replication. It was also learned that inoculation of 7-day-old embryos causes growth retardation and lesions. The potential of CAV to cause immunosuppression was further examined using CTL responses to REV. CTL were obtained from chickens between 36 and 44 days of age with REV and CAV given at different time points. In contrast to our earlier studies, in these experiments we were unable to detect a direct impact of CAV on REV-specific CTL, perhaps because the CTL were obtained from older birds. Inoculation of CAV at one day of age decreased the IgG antibody responses to inactivated STM administered at 10 days of age. 4. Scientific and Agricultural Implications The impact of the research was especially important for the poultry industry in Israel. The producers have been educated on the importance of the disease through the many presentations. It is now well known to the stakeholders that CAV can aggravate other diseases, decrease productivity and profitability. As a consequence they monitor the antibody status of the breeders so that the maternal antibody status of the broilers is known. Also vaccination of breeder flock that remain antibody negative may become feasible further reducing the negative impact of CAV infection. Vaccination may become more important because improved biosecurity of the breeder flocks to prevent avian influenza and Salmonella may delay the onset of seroconversion for CAV by natural exposure resulting in CAV susceptible broilers lacking maternal antibodies. Scientifically, the research added important information on the horizontal spread of CAV through feathers, the interactions with Salmonella typhimurium and the demonstration that antigen-antibody complex vaccines may provide protective immunity.
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