Academic literature on the topic 'Blys'

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Journal articles on the topic "Blys"

1

Scapini, Patrizia, Bernardetta Nardelli, Gianpaolo Nadali, et al. "G-CSF–stimulated Neutrophils Are a Prominent Source of Functional BLyS." Journal of Experimental Medicine 197, no. 3 (2003): 297–302. http://dx.doi.org/10.1084/jem.20021343.

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B lymphocyte stimulator (BLyS) is a novel member of the TNF ligand superfamily that is important in B cell maturation and survival. We demonstrate that human neutrophils, after incubation with G-CSF or, less efficiently, IFNγ, express high levels of BLyS mRNA and release elevated amounts of biologically active BLyS. In contrast, surface expression of the membrane-bound BLyS was not detected in activated neutrophils. Indeed, in neutrophils, uniquely among other myeloid cells, soluble BLyS is processed intracellularly by a furin-type convertase. Worthy of note, the absolute capacity of G-CSF–sti
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2

Goenka, Radhika, Andrew H. Matthews, Bochao Zhang, et al. "Local BLyS production by T follicular cells mediates retention of high affinity B cells during affinity maturation." Journal of Experimental Medicine 211, no. 1 (2013): 45–56. http://dx.doi.org/10.1084/jem.20130505.

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We have assessed the role of B lymphocyte stimulator (BLyS) and its receptors in the germinal center (GC) reaction and affinity maturation. Despite ample BLyS retention on B cells in follicular (FO) regions, the GC microenvironment lacks substantial BLyS. This reflects IL-21–mediated down-regulation of the BLyS receptor TACI (transmembrane activator and calcium modulator and cyclophilin ligand interactor) on GC B cells, thus limiting their capacity for BLyS binding and retention. Within the GC, FO helper T cells (TFH cells) provide a local source of BLyS. Whereas T cell–derived BLyS is dispens
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3

Chang, Sook Kyung, Bonnie K. Arendt, Jaime R. Darce, Xiaosheng Wu, and Diane F. Jelinek. "A role for BLyS in the activation of innate immune cells." Blood 108, no. 8 (2006): 2687–94. http://dx.doi.org/10.1182/blood-2005-12-017319.

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AbstractB-lymphocyte stimulator (BLyS) is a member of the tumor necrosis factor (TNF) ligand superfamily. Although BLyS costimulates adaptive immune cells, the ability of BLyS to stimulate innate immune cells has not been described. Here, we show that BLyS strongly induces human monocyte survival, and activation as measured by proinflammatory cytokine secretion and up-regulation of costimulatory molecule expression. In addition, monocytes cultured with BLyS differentiated into macrophage-like cells. Regarding BLyS receptor(s) expression, freshly isolated monocytes bound low levels of exogenous
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4

Elsawa, Sherine F., Anne J. Novak, Deanna M. Grote, et al. "B-lymphocyte stimulator (BLyS) stimulates immunoglobulin production and malignant B-cell growth in Waldenström macroglobulinemia." Blood 107, no. 7 (2006): 2882–88. http://dx.doi.org/10.1182/blood-2005-09-3552.

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AbstractWaldenström macroglobulinemia (WM) is a serious and frequently fatal B-cell malignancy associated with an elevated monoclonal IgM protein in the serum. Many of the mechanisms leading to this disease are not yet known. B-lymphocyte stimulator (BLyS) is a TNF family member that is critical for maintenance of normal B-cell development and homeostasis. BLyS is overexpressed in a variety of B-cell malignancies and has been shown to inhibit apoptosis in malignant B cells. It also regulates immunoglobulin secretion by normal B cells. To determine the relevance of BLyS in WM, we examined the
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5

Novak, Anne J., Deanna M. Grote, Mary Stenson, et al. "Expression of BLyS and its receptors in B-cell non-Hodgkin lymphoma: correlation with disease activity and patient outcome." Blood 104, no. 8 (2004): 2247–53. http://dx.doi.org/10.1182/blood-2004-02-0762.

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Abstract BLyS, recently shown to be critical for survival of normal B cells, has been found to be elevated in a number of immune disease models. A role for BLyS in the survival of malignant B cells has also been revealed and we therefore sought to identify a role for BLyS and its receptors in non-Hodgkin lymphoma (NHL). We found that tumor cells from all NHL histologic subtypes expressed one or more of 3 known receptors (BCMA, TACI, and BAFF-R) for BLyS; however, the pattern of expression was variable. We provide evidence that BLyS is expressed in tumors from patients with NHL and that BLyS le
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6

Nardelli, Bernardetta, Ornella Belvedere, Viktor Roschke, et al. "Synthesis and release of B-lymphocyte stimulator from myeloid cells." Blood 97, no. 1 (2001): 198–204. http://dx.doi.org/10.1182/blood.v97.1.198.

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Abstract B-lymphocyte stimulator (BLyS) is a recently identified novel member of the tumor necrosis factor ligand superfamily shown to exist in a membrane-bound and soluble form. BLyS was found to be specifically expressed on cells of myeloid lineage and to selectively stimulate B-lymphocyte proliferation and immunoglobulin production. The expression of a cytokine involved in potentiation of humoral immune responses, such as BLyS, is expected to be strictly controlled. The goal of the present study was to examine regulation of BLyS levels in monocytic cells in response to cytokines and during
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7

Ansell, Stephen M., Deanna M. Grote, Steven C. Ziesmer, Thomas E. Witzig, Robert A. Kyle, and Anne J. Novak. "B-Lymphocyte Stimulator (BLyS) Is Highly Expressed in Waldenstrom’s Macroglobulinemia." Blood 104, no. 11 (2004): 2291. http://dx.doi.org/10.1182/blood.v104.11.2291.2291.

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Abstract Waldenstrom’s macroglobulinemia is a serious and frequently fatal illness, however many of the mechanisms leading to this disease are not yet known. It is clear, however, that there is dysregulation of the balance between cell proliferation and programmed cell death. BLyS (B-lymphocyte stimulator) is a newly identified TNF family member expressed by monocytes, macrophages, and dendritic cells. BLyS has been shown to be critical for maintenance of normal B cell development and homeostasis, and has been found to stimulate lymphocyte growth. BLyS is overexpressed in a variety of B-cell m
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8

Weitzman, Jonathan B. "Absolute BlyS." Genome Biology 2 (2001): spotlight—20010822–01. http://dx.doi.org/10.1186/gb-spotlight-20010822-01.

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9

Novak, Anne J., Deanna M. Grote, Steven C. Ziesmer, et al. "Elevated BLyS Levels in Patients with Familial and Sporadic B-CLL: Correlation with BLyS Polymorphisms." Blood 104, no. 11 (2004): 964. http://dx.doi.org/10.1182/blood.v104.11.964.964.

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Abstract Serum BLyS levels have been found to be elevated in a number of immune disease models and there is increasing evidence that this may correlate with pathogenesis of various B cell related disorders including B cell malignancies. While it is clear that BLyS expression is required for normal B cell development and homeostasis, the exact source of BLyS in these scenarios and definition of the mechanisms that control BLyS expression remain to be fully elucidated. Serum BLyS levels are elevated in a number of B cell malignancies known to have a familial incidence. Therefore, we sought to de
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10

Elsawa, Sherine F., Anne J. Novak, Deanna M. Grote, et al. "Role of B-Lymphocyte Stimulator (BLyS) in Waldenstrom’s Macroglobulinemia." Blood 106, no. 11 (2005): 601. http://dx.doi.org/10.1182/blood.v106.11.601.601.

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Abstract Waldenstrom’s macroglobulinemia (WM) is a serious and frequently fatal disorder characterized by the production of a monoclonal IgM protein, a lymphoplasmacytic infiltrate in the bone marrow, and associated symptoms including anemia, lymphadenopathy and hyperviscosity. Many of the mechanisms leading to this disease are not yet known. It is clear, however, that there is dysregulation of the balance between cell proliferation and programmed cell death. BLyS (B-lymphocyte stimulator) is a TNF family member expressed by monocytes, neutrophils, macrophages, and dendritic cells. BLyS has be
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