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Journal articles on the topic 'Blys'

Author: Grafiati
Published: 4 June 2021
Last updated: 9 March 2023

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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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11

Goenka, Radhika, Andrew Mathews, Patrick O'Neill, et al. "Positive selection during affinity maturation relies on T cell derived BLyS (61.3)." Journal of Immunology 186, no. 1_Supplement (2011): 61.3. http://dx.doi.org/10.4049/jimmunol.186.supp.61.3.

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Abstract Protective humoral immunity relies on high affinity B cell clones that are generated and selected during the germinal center (GC) reaction. To determine whether BLyS family member(s) play a role in this process, we assessed their distribution within the GC. We show that majority of the GC is devoid of BLyS despite the presence of ample BLyS in the adjacent follicular regions. The paucity of BLyS correlates with down-regulation of TACI receptor on GC B cells and likewise follicular B cells in TACI-deficient mice bind less BLyS. TACI down-regulation on follicular B cells is mediated by
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12

Crowley, Jenni E., Jason E. Stadanlick, John C. Cambier та Michael P. Cancro. "FcγRIIB signals inhibit BLyS signaling and BCR-mediated BLyS receptor up-regulation". Blood 113, № 7 (2009): 1464–73. http://dx.doi.org/10.1182/blood-2008-02-138651.

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Abstract These studies investigate how interactions between the BCR and FcγRIIB affect B lymphocyte stimulator (BLyS) recep-tor expression and signaling. Previous studies showed that BCR ligation up-regulates BLyS binding capacity in mature B cells, reflecting increased BLyS receptor levels. Here we show that FcγRIIB coaggregation dampens BCR-induced BLyS receptor up-regulation. This cross-regulation requires BCR and FcγRIIB coligation, and optimal action relies on the Src-homology-2 (SH2)–containing inositol 5 phosphase-1 (SHIP1). Subsequent to FcγRIIB/BCR coaggregation, the survival promotin
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13

Fu, Lingchen, Yen-Chiu Lin-Lee, Lan V. Pham, Archito Tamayo, Linda Yoshimura та Richard J. Ford. "Constitutive NF-κB and NFAT activation leads to stimulation of the BLyS survival pathway in aggressive B-cell lymphomas". Blood 107, № 11 (2006): 4540–48. http://dx.doi.org/10.1182/blood-2005-10-4042.

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AbstractB-lymphocyte stimulator (BLyS), a relatively recently recognized member of the tumor necrosis factor ligand family (TNF), is a potent cell-survival factor expressed in many hematopoietic cells. BLyS binds to 3 TNF-R receptors, TACI, BCMA, BAFF-R, to regulate B-cell survival, differentiation, and proliferation. The mechanisms involved in BLYS gene expression and regulation are still incompletely understood. In this study, we examined BLYS gene expression, function, and regulation in B-cell non-Hodgkin lymphoma (NHL-B) cells. Our studies indicate that BLyS is constitutively expressed in
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14

Woodland, Robert T., Casey J. Fox, Madelyn R. Schmidt, et al. "Multiple signaling pathways promote B lymphocyte stimulator–dependent B-cell growth and survival." Blood 111, no. 2 (2008): 750–60. http://dx.doi.org/10.1182/blood-2007-03-077222.

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We investigated the mechanism by which B lymphocyte stimulator (BLyS)/BAFF, a tumor necrosis factor superfamily ligand, promotes B-cell survival and resistance to atrophy. BLyS stimulation activates 2 independent signaling pathways, Akt/mTOR and Pim 2, associated with cell growth and survival. BLyS blocks the cell volume loss (atrophy) that freshly isolated B cells normally undergo when maintained in vitro while concurrently increasing glycolytic activity and overall metabolism. This atrophy resistance requires Akt/mTOR. We used a genetic approach to resolve the contributions of Akt/mTOR and P
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15

Landau, D.-A., M. Rosenzwajg, D. Saadoun, D. Klatzmann, and P. Cacoub. "The B lymphocyte stimulator receptor–ligand system in hepatitis C virus-induced B cell clonal disorders." Annals of the Rheumatic Diseases 68, no. 3 (2008): 337–44. http://dx.doi.org/10.1136/ard.2007.085910.

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Objective:The study aim was to examine the B lymphocyte stimulator (BLyS) receptor–ligand system in hepatitis C virus (HCV)-induced B lymphocyte clonal disorders.Methods:94 patients with chronic HCV (including 35 with HCV+ mixed cryoglobulinaemia (MC)-vasculitis and nine with HCV+ B cell non-Hodgkin’s lymphoma (B-NHL)) and 15 healthy volunteers were included.Results:A twofold serum BLyS increase was associated with HCV-induced MC-vasculitis, and a threefold increase with HCV-induced B-NHL, compared with patients that were HCV+, but without vasculitis, or healthy controls (p<0.05). Lower mem
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16

Scholz, Jean, Bapi Pahar, Joanna B. Madej, et al. "Effects of temporary BLyS treatment of rhesus macaques." Journal of Immunology 198, no. 1_Supplement (2017): 215.19. http://dx.doi.org/10.4049/jimmunol.198.supp.215.19.

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Abstract BLyS is a survival cytokine that regulates peripheral B cell numbers and transitional B cell throughput. In mice, exogenous BLyS administration yields elevated pre-immune B cell numbers, an increased proportional representation of transitional B cells, and shifts in repertoire composition (1–3). Consistent with these observations, BLyS pretreatment alters the quality of antibody responses to HIV gp140 in mice, yielding enhanced neutralizing responses (4). While it is assumed that BLyS plays analogous roles in other species, similar studies in nonhuman primates are lacking. Accordingly
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17

Crowley, Jenni Eileen, Jean L. Scholz, Thi-Sau Migone, and Michael P. Cancro. "Primary and memory B cells occupy independent homeostatic niches (B20)." Journal of Immunology 178, no. 1_Supplement (2007): LB4. http://dx.doi.org/10.4049/jimmunol.178.supp.b20.

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Abstract The cytokines BLyS (B lymphocyte stimulator) and APRIL (a proliferation-inducing ligand) interact with three receptors – BR3, TACI, and BCMA – to regulate peripheral B cell homeostasis. Experimental evidence indicates that the BLyS-BR3 interaction governs the size and composition of primary B cell subsets by controlling the proportion of transitional (TR) cells that complete differentiation and determining the lifespan of follicular (FO) and marginal zone (MZ) B cells. The role of the BLyS family in the regulation and maintenance of memory B cell subsets remains less understood. Accor
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18

Novak, Anne J., Deanna M. Grote, Steven C. Ziesmer, et al. "Elevated Serum B-Lymphocyte Stimulator Levels in Patients With Familial Lymphoproliferative Disorders." Journal of Clinical Oncology 24, no. 6 (2006): 983–87. http://dx.doi.org/10.1200/jco.2005.02.7938.

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Purpose Serum B-lymphocyte stimulator (BLyS) levels have been found to be elevated in a number of immune disease models. Therefore, we sought to establish whether BLyS levels were elevated in patients with B-cell lymphoproliferative disorders and to determine whether elevated BLyS levels correlated with clinical characteristics of the disease. Patients and Methods Specimens were collected from the peripheral blood of individuals diagnosed with B-cell chronic lymphocytic leukemia (B-CLL; n = 70) or from age- and sex-matched patients seen at the same institution (n = 41). Serum BLyS levels were
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19

Oki, Yasuhiro, Georgios V. Georgakis, Thi-Sau Migone, Larry W. Kwak, and Anas Younes. "Serum BLyS Level as a Prognostic Marker in Patients with Lymphoma." Blood 106, no. 11 (2005): 1926. http://dx.doi.org/10.1182/blood.v106.11.1926.1926.

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Abstract Background: BLyS is a TNF family member which was recently shown to play a critical role for survival of normal and malignant B cells. BLyS is expressed by monocytes, macrophages, dendritic cells as well as lymphoma cells, where its expression levels increase as tumors transform to a more aggressive phenotype. Previous small studies suggested that serum BLyS level is elevated in some proportion of patients with aggressive non-Hodgkin lymphoma (NHL). Little is known if serum BLyS level has prognostic value in patients with lymphoma. Thus, we determined serum soluble BLyS levels in 191
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20

Novak, Anne J., Susan L. Slager, Steven C. Ziesmer, et al. "Polymorphisms in the BLyS Gene Are Associated with an Increased Risk of Developing B-Cell Non-Hodgkin Lymphoma." Blood 110, no. 11 (2007): 564. http://dx.doi.org/10.1182/blood.v110.11.564.564.

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Abstract Background: Elevated serum BLyS levels have been found in patients with both malignant and autoimmune diseases when compared to those of healthy donors, suggesting that BLyS may play a pathogenic role. While it is clear that BLyS expression is required for normal B cell development and homeostasis, the mechanistic details underlying control of BLyS expression remain to be defined. In previous work we found that a single nucleotide polymorphisms (SNP) in the BLyS promoter (−871C→T) resulted in increased BLyS transcription suggesting that genetic variation in the BLyS gene may influence
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21

Kyrtsonis, Marie-Christine, Katerina Sarris, Efstathios Koulieris, et al. "Serum Soluble TACI, a BLyS Receptor, Is a Powerful Prognostic Marker of Outcome in Chronic Lymphocytic Leukemia." BioMed Research International 2014 (2014): 1–5. http://dx.doi.org/10.1155/2014/159632.

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BLyS is involved in CLL biology and its low soluble serum levels related to a shorter time to first treatment (TFT). TACI is a BLyS receptor and can be shed from cells’ surface and circulate in soluble form (sTACI). We investigated the impact of serum BLyS and sTACI levels at diagnosis in CLL patients and their relationship with disease parameters and patients’ outcome. Serum BLyS was determined in 73 patients, while sTACI in 60. Frozen sera drawn at diagnosis were tested by ELISA. sTACI concentrations correlated with BLyS (P=-0.000021), b2-microglobulin (P=0.005), anemia (P=-0.03), thrombocyt
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22

Briones, J. "BLyS and BLyS receptor expression in non-Hodgkin's lymphoma." Experimental Hematology 30, no. 2 (2002): 135–41. http://dx.doi.org/10.1016/s0301-472x(01)00774-3.

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23

Fu, Lingchen, Tamayo Archito, Yen-Chiu Lin-Lee, Lan Pham, Linda Yoshimura, and Richard J. Ford. "The BLyS Survival Pathway in NHL-B Cells: Constitutive NF-kB and NFAT Lead to Activation." Blood 104, no. 11 (2004): 2279. http://dx.doi.org/10.1182/blood.v104.11.2279.2279.

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Abstract B-cell non-Hodgkin’s Lymphomas (NHL-B), neoplasms of the immune system have shown a significant increase in incidence in the USA over the last three decades. While the pathophysiology of the NHL-B is still unclear, the need to identify the relevant genes and critical signaling pathways, and their involvement in the disease processes in NHL-B have begun to be elucidated. Recently, B Lymphocyte Stimulator (BLyS) has been described as a relatively new member of the TNF ligand family, as a potent cell survival factor that is expressed in many hematopoietic cells, including neoplastic B ce
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24

Do, Richard K. G., Eunice Hatada, Hayyoung Lee, Michelle R. Tourigny, David Hilbert, and Selina Chen-Kiang. "Attenuation of Apoptosis Underlies B Lymphocyte Stimulator Enhancement of Humoral Immune Response." Journal of Experimental Medicine 192, no. 7 (2000): 953–64. http://dx.doi.org/10.1084/jem.192.7.953.

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B lymphocyte stimulator (BLyS) is a newly identified monocyte-specific TNF family cytokine. It has been implicated in the development of autoimmunity, and functions as a potent costimulator with antiimmunoglobulin M in B cell proliferation in vitro. Here we demonstrate that BLyS prominently enhances the humoral responses to both T cell–independent and T cell–dependent antigens, primarily by attenuation of apoptosis as evidenced by the prolonged survival of antigen-activated B cells in vivo and in vitro. BLyS acts on primary splenic B cells autonomously, and directly cooperates with CD40 ligand
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25

Scholz, Jean L., Jenni E. Crowley, Patrick J. O’Neill, et al. "The effect of BLyS neutralization on primary B cell compartments and responses (B31)." Journal of Immunology 178, no. 1_Supplement (2007): LB6—LB7. http://dx.doi.org/10.4049/jimmunol.178.supp.b31.

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Abstract B lymphocyte stimulator (BLyS) controls the proportion of transitional B cells completing differentiation and the longevity of most primary B cells. These key roles in B cell selection, survival and homeostasis make BLyS and its receptors attractive candidates for targeted B cell therapeutics. Here we have used a neutralizing hamster anti-mouse BLyS antibody to assess how BLyS depletion influences developing and primary B cell subsets, as well as how this treatment impacts primary TD and TI immune responses. Mice treated with 10F4 show rapid and substantial reductions in the transitio
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26

Santos, Daniel Ditzel, Olivier Tournilhac, Lian Xu, et al. "B-Lymphocyte Stimulator Protein (BLYS) Is Expressed by Bone Marrow Mast and Lymphoplasmacytic Cells in Waldenstrom’s Macroglobulinemia, and Provides Signaling for Growth, Survival and IgM Secretion." Blood 104, no. 11 (2004): 3358. http://dx.doi.org/10.1182/blood.v104.11.3358.3358.

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Abstract B-lymphocyte stimulator protein (BLYS) is a member of the tumor necrosis family of ligands which is expressed by monocytes and neutrophils and regulates B-cell homeostasis and immunoglobulin production through its receptors BCMA, TACI and BAFF-R. In recent studies, we have shown that bone marrow (BM) mast cells (MC) are increased in WM patients and support tumor cell growth. We therefore evaluated sorted WM BM MC (CD117+FceRI+) and lymphoplasmacytic cells (LPC) for BLYS, BCMA, TACI AND BAFF-R by multicolor flow cytometry and RT-PCR. Results were as follows: Flow Cytometry RT-PCR WM MC
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27

Nimmanapalli, Ramadevi, Mi-Ae Lyu, Min Du, Michael J. Keating, Michael G. Rosenblum, and Varsha Gandhi. "The growth factor fusion construct containing B-lymphocyte stimulator (BLyS) and the toxin rGel induces apoptosis specifically in BAFF-R–positive CLL cells." Blood 109, no. 6 (2006): 2557–64. http://dx.doi.org/10.1182/blood-2006-08-042424.

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Abstract The cytokine B lymphocyte stimulator (BLyS) mediates its effect through cell-surface receptors BAFF-R, TACI, and BCMA. BLyS receptors are expressed only on B cells and not present in other normal cells including normal T lymphocytes. Chronic lymphocytic leukemia (CLL) is a B-cell disease and CLL lymphocytes express BLyS receptors. Gelonin, a type 1 ribosome-inactivating toxin, lacks cell membrane binding domain and hence is nontoxic to intact cells. We generated a construct of recombinant gelonin (rGel) fused to BLyS to specifically target quiescent B-CLL lymphocytes. The construct rG
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Chang, Sook Kyung, and Diane F. Jelinek. "BLyS Regulates Human Myeloma Cell IL-6 Expression." Blood 104, no. 11 (2004): 1412. http://dx.doi.org/10.1182/blood.v104.11.1412.1412.

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Abstract Multiple myeloma (MM) is a malignant disease of plasma cells that accumulate in the bone marrow. The survival mechanisms of myeloma cells are still not fully understood. There are several cytokines that are known to support the survival and growth of myeloma cells, such as IL-6, IGF-I, TNF-a, and IL-1β. Recent evidence has also shown that the TNF family member, B lymphocyte stimulator (BLyS), is critical for normal B cell development and homeostasis, as well as for survival of malignant B cells, including MM. However, it should be noted that the precise mechanisms by which BLyS promot
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29

Dolff, S., and J. Menke. "BLyS und Belimumab." Der Nephrologe 9, no. 3 (2014): 233–35. http://dx.doi.org/10.1007/s11560-013-0812-6.

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Bath, Natalie M., Bret M. Verhoven, Nancy A. Wilson, et al. "APRIL/BLyS deficient rats prevent donor specific antibody (DSA) production and cell proliferation in rodent kidney transplant model." PLOS ONE 17, no. 10 (2022): e0275564. http://dx.doi.org/10.1371/journal.pone.0275564.

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APRIL (A proliferation inducing ligand) and BLyS (B Lymphocyte Stimulator) are two critical survival factors for B lymphocytes and plasma cells, the main source of alloantibody. We sought to characterize the specific effects of these cytokines in a kidney transplant model of antibody mediated rejection (AMR). We engineered APRIL-/- and BLyS-/- Lewis rats using CRISPR/Cas9. APRIL-/- and BLyS-/- rats were sensitized with Brown Norway (BN) blood (complete MHC mismatch). Twenty-one days following sensitization, animals were harvested and collected tissues were analyzed using flow cytometry, ELISPO
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Landau, Dan Avi, Michelle Rosenzwajg, David Saadoun, David Klatzmann, and Patrice Cacoub. "The BLyS/BAFF Receptor-Ligand System in HCV Induced B-Cell Clonal Disorders." Blood 110, no. 11 (2007): 3866. http://dx.doi.org/10.1182/blood.v110.11.3866.3866.

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Abstract The study aim was to examine the B-Lymphocytes Stimulator (BLyS) receptor-ligand system in HCV induced B lymphocyte clonal disorders. 94 patients with chronic HCV [including 35 HCV+ mixed cryoglobulinemia (MC)-vasculitis and 9 HCV+ B-non Hodgkin’s lymphoma (B-NHL) patients] and 15 healthy volunteers were included. A 2-fold serum BLyS increase was associated with HCV-induced MC-vasculitis, and a three-fold increase with HCV-induced B-NHL, compared with HCV+ patients without vasculitis or healthy controls (p<0.05). Lower mBLyS expression in HCV-induced MC vasculitis was observed. CD1
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Scapini, Patrizia, Antonio Carletto, Bernardetta Nardelli, et al. "Proinflammatory mediators elicit secretion of the intracellular B-lymphocyte stimulator pool (BLyS) that is stored in activated neutrophils: implications for inflammatory diseases." Blood 105, no. 2 (2005): 830–37. http://dx.doi.org/10.1182/blood-2004-02-0564.

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Abstract We have recently shown that granulocyte–colony-stimulating factor (G-CSF)– and interferon-γ (IFN-γ)–activated human neutrophils accumulate and release remarkable amounts of soluble B-lymphocyte stimulator (BLyS) in vitro. In this study, we provide evidence that neutrophils migrating into skin window exudates (SWEs) developed in healthy volunteers and in patients with rheumatoid arthritis (RA), synthesized, and released BLyS in response to locally produced G-CSF. Accordingly, the concentrations of soluble BLyS in SWEs were significantly more elevated than in serum. Because the levels o
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33

Scholz, Jean L., Jenni E. Crowley, Mary M. Tomayko, et al. "BLyS inhibition eliminates primary B cells but leaves natural and acquired humoral immunity intact." Proceedings of the National Academy of Sciences 105, no. 40 (2008): 15517–22. http://dx.doi.org/10.1073/pnas.0807841105.

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We have used an inhibiting antibody to determine whether preimmune versus antigen-experienced B cells differ in their requisites for BLyS, a cytokine that controls differentiation and survival. Whereas in vivo BLyS inhibition profoundly reduced naïve B cell numbers and primary immune responses, it had a markedly smaller effect on memory B cells and long-lived plasma cells, as well as secondary immune responses. There was heterogeneity within the memory pools, because IgM-bearing memory cells were sensitive to BLyS depletion whereas IgG-bearing memory cells were not, although both were more res
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Doshi, Bhavya S., Robert J. Davidson, and Valder R. Arruda. "The Un-BLyS-Ful State: Blocking Factor VIII Inhibitor Development with BLyS Depletion." Blood 132, Supplement 1 (2018): 138. http://dx.doi.org/10.1182/blood-2018-99-114795.

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Abstract The development of neutralizing alloantibodies (inhibitors) to infused factor VIII (FVIII) remains the most significant complication of therapy in hemophilia A (HA). Despite some insights into genetic and environmental risk factors associated with inhibitor development, the immunological mechanisms behind this complication remain incompletely understood. Given that infused FVIII is likely encountered in the periphery, transitional B cell response to FVIII may regulate inhibitor development. Transitional B cell survival, maturation and proliferation are tightly regulated by the cytokin
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35

Novak, Anne J., Richard J. Bram, Neil E. Kay, and Diane F. Jelinek. "Aberrant expression of B-lymphocyte stimulator by B chronic lymphocytic leukemia cells: a mechanism for survival." Blood 100, no. 8 (2002): 2973–79. http://dx.doi.org/10.1182/blood-2002-02-0558.

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B-cell chronic lymphocytic leukemia (B-CLL) is defined by the accumulation of CD5+ B cells in the periphery and bone marrow. This disease is not characterized by highly proliferative cells but rather by the presence of leukemic cells with significant resistance to apoptosis and, therefore, prolonged survival. B-lymphocyte stimulator (BLyS) is a newly identified tumor necrosis factor (TNF) family member shown to be critical for maintenance of normal B-cell development and homeostasis and it shares significant homology with another TNF superfamily member, APRIL. The striking effects of BLyS on n
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36

Adamia, Sophia, Lian Xu, Antonio Sacco, and Steven Treon. "Identification Genetic Variations (GVs) Causing Splicing of TNF Family Members and Adaptor Proteins That Modulate NFkB Pathways in Waldenstrom’s Maroglobulinemia (WM)." Blood 110, no. 11 (2007): 2516. http://dx.doi.org/10.1182/blood.v110.11.2516.2516.

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Abstract The TNF ligand-receptor superfamily and their adaptor proteins regulate important B-cell signaling pathways, including CD40L-CD40 and APRIL/BLYS-TACI through adaptor protein TRAF2. These pathways promote B-cell differentiation and immunoglobulin heavy chain class switching. Defects in immunoglobulin heavy chain class switching and presence of constitutive IgA and IgG hypogammaglobulinemia in patients with WM have previously been reported by us (Hunter et al, ASH2006). In WM patients we identified several novel splice variants of TNF-family members CD40 and BLYS, and their adaptor prot
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37

Fontaine, Julie, Josiane Chagnon-Choquet, Han Sang Valcke, Johanne Poudrier, and Michel Roger. "High expression levels of B lymphocyte stimulator (BLyS) by dendritic cells correlate with HIV-related B-cell disease progression in humans." Blood 117, no. 1 (2011): 145–55. http://dx.doi.org/10.1182/blood-2010-08-301887.

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AbstractIn view of assessing the possible contribution of dendritic cells (DCs) to HIV-related B-cell disorders, we have longitudinally measured B lymphocyte stimulator (BLyS) surface expression by myeloid DCs (mDCs) and concentrations of B-cell growth factors in the blood of subjects undergoing primary HIV infection with different rates of disease progression. We report that BLyS surface expression by mature mDCs and precursors as well as blood levels of BLyS, a proliferation-inducing ligand (APRIL), interleukin-6 (IL-6), and IL-10 increased above normal levels in both rapid and normal HIV pr
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38

Zekavat, Ghazal, Thi-Sau Migone, Robert E. Roses, Michael P. Cancro, Ali Naji, and Hooman Noorchashm. "The Impact of B Lymphocyte Depletion on the Pathogenesis of Autoimmune Diabetes (131.28)." Journal of Immunology 178, no. 1_Supplement (2007): S243. http://dx.doi.org/10.4049/jimmunol.178.supp.131.28.

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Abstract NOD B cell development is characterized by a defective homeostatic checkpoint in B cell maturation and selection. Having demonstrated that the progression of autoimmune diabetes requires antigen presentation by B-lymphocytes, we hypothesized that B cell depletion may prevent diabetes progression in NOD mice. Here, we employed two distinct approaches for in vivo B lymphocyte depletion: a cohort of adult hCD20 Tg NOD mice were treated with the B lymphocyte depleting mAb, Rituximab (anti-CD20) anda cohort of adult NOD mice were treated with a neutralizing Hamster anti-mouse mAb specific
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39

Novak, Anne J., Jaime R. Darce, Bonnie K. Arendt, et al. "Expression of BCMA, TACI, and BAFF-R in multiple myeloma: a mechanism for growth and survival." Blood 103, no. 2 (2004): 689–94. http://dx.doi.org/10.1182/blood-2003-06-2043.

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Abstract Multiple myeloma (MM) is a progressive disease that is thought to result from multiple genetic insults to the precursor plasma cell that ultimately affords the tumor cell with proliferative potential despite its differentiated phenotype and resistance to undergoing apoptosis. Altered expression of antiapoptotic factors as well as growth factors have been described in a significant number of patients. However, the key regulatory elements that control myeloma development and progression remain largely undefined. Because of the knowledge that B-lymphocyte stimulator (BLyS), a tumor necro
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40

Varfolomeev, Eugene, Frank Kischkel, Flavius Martin, et al. "APRIL-Deficient Mice Have Normal Immune System Development." Molecular and Cellular Biology 24, no. 3 (2004): 997–1006. http://dx.doi.org/10.1128/mcb.24.3.997-1006.2004.

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ABSTRACT APRIL (a proliferation-inducing ligand) is a member of the tumor necrosis factor (TNF) superfamily. APRIL mRNA shows high levels of expression in tumors of different origin and a low level of expression in normal cells. APRIL shares two TNF receptor family members, TACI and BCMA, with another TNF homolog, BLyS/BAFF. BLyS is involved in regulation of B-cell activation and survival and also binds to a third receptor, BR3/BAFF-R, which is not shared with APRIL. Recombinant APRIL and BLyS induce accumulation of B cells in mice, while BLyS deficiency results in severe B-cell dysfunction. T
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41

Hondowicz, B. D., S. T. Alexander, W. J. Quinn, et al. "The role of BLyS/BLyS receptors in anti-chromatin B cell regulation." International Immunology 19, no. 4 (2007): 465–75. http://dx.doi.org/10.1093/intimm/dxm011.

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42

Liu, Mei-Yun, Wei Han, Yan-Li Ding, et al. "Generation and Characterization of C305, a Murine Neutralizing scFv Antibody That Can Inhibit BLyS Binding to Its Receptor BCMA." Acta Biochimica et Biophysica Sinica 37, no. 6 (2005): 415–20. http://dx.doi.org/10.1111/j.1745-7270.2005.00059.x.

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Abstract B-lymphocyte stimulator (BLyS) is a member of the tumor necrosis factor (TNF) family and a key regulator of B cell response. Neutralizing single-chain fragment variable (scFv) antibody against BLyS binding to its receptor BCMA has the potential to play a prominent role in autoimmune disease therapy. A phage display scFv library constructed on pIII protein of M13 filamentous phage was screened using BLyS. After five rounds of panning, their binding activity was characterized by phage-ELISA. Nucleotide sequencing revealed that at least two different scFv gene fragments (C305 and D416) w
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43

Fu, Lingchen, Yen-Chiu Lin-Lee, Archito Tamayo, Linda Yoshimura, and Richard J. Ford. "BAFF-R Receptor Also Functions in the Nucleus of Normal and Neoplastic Human B Lymphocytes." Blood 108, no. 11 (2006): 2368. http://dx.doi.org/10.1182/blood.v108.11.2368.2368.

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Abstract B-lymphocyte stimulator (BLyS) is a relatively newly described tumor necrosis factor (TNF) superfamily cytokine involved in cell survival and proliferation in normal and neoplastic B cells, particularly in the aggressive B cell non-Hodgkin’s lymphomas (NHL-B). BLyS binds to three receptors: BAFF-R (or BR3), BCMA and TACI. However, recent studies have shown that BLyS regulates B cell survival and proliferation predominately through BAFF-R. Mice with mutant BAFF-R show significant decrease in the peripheral blood B-lymphocyte compartment, similar to the phenotype of BLyS knockout mice.
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44

Scholz, Jean, Martina Soldemo, Pia Dosenovic, et al. "Potentially neutralizing B cell clonotypes are eliminated at peripheral selection checkpoints (LYM6P.768)." Journal of Immunology 192, no. 1_Supplement (2014): 131.5. http://dx.doi.org/10.4049/jimmunol.192.supp.131.5.

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Abstract B lymphocyte stimulator (BLyS) signals via BR3 mediate selection and survival in the transitional, mature, and germinal center B cell pools. We have previously shown that treatment of mice with exogenous BLyS prior to immunization with HIV-1 envelope (Env) trimers improves neutralizing antibody breadth and potency. We are therefore investigating the hypothesis that broadly neutralizing B cell clonotypes are rare because of counter-selection at the transitional or germinal center checkpoints. Here we show that Env-specific murine B cells in pre-immune, germinal center, and memory B cel
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45

Li, Xinrui, Kaihong Su, Alexander J. Szalai, Tong Zhou, Robert P. Kimberly, and Jeffrey C. Edberg. "Immune opsonins modulate BLyS/BAFF release in a receptor-specific fashion (53.6)." Journal of Immunology 178, no. 1_Supplement (2007): S104. http://dx.doi.org/10.4049/jimmunol.178.supp.53.6.

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Abstract TNF ligand superfamily member 13B (B lymphocyte stimulator (BLyS), B cell activating factor (BAFF)) promotes primary B cell proliferation and immunoglobulin production. It exists in both membrane-bound and soluble forms. Because the soluble form is thought to be the primary biologically active form, we investigated factors that might regulate its cleavage and processing. In both myeloid cell lines and primary human monocytes, the shedding of membrane BLyS can be regulated by CRP and IgG. Within 10 minutes, both of these opsonins trigger significant shedding of BLyS (up to 52.2±3.0%, p
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46

Woodland, Robert T., Madelyn R. Schmidt, and Craig B. Thompson. "BLyS and B cell homeostasis." Seminars in Immunology 18, no. 5 (2006): 318–26. http://dx.doi.org/10.1016/j.smim.2006.06.001.

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47

O'Connor, Brian P., Vanitha S. Raman, Loren D. Erickson, et al. "BCMA Is Essential for the Survival of Long-lived Bone Marrow Plasma Cells." Journal of Experimental Medicine 199, no. 1 (2004): 91–98. http://dx.doi.org/10.1084/jem.20031330.

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Long-lived humoral immunity is manifested by the ability of bone marrow plasma cells (PCs) to survive for extended periods of time. Recent studies have underscored the importance of BLyS and APRIL as factors that can support the survival of B lineage lymphocytes. We show that BLyS can sustain PC survival in vitro, and this survival can be further enhanced by interleukin 6. Selective up-regulation of Mcl-1 in PCs by BLyS suggests that this α-apoptotic gene product may play an important role in PC survival. Blockade of BLyS, via transmembrane activator and cyclophilin ligand interactor–immunoglo
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48

Stadanlick, Jason E., Jean L. Scholz, Juli P. Miller, and Michael P. Cancro. "BCR Signaling Generates NF-kB2 (p100) For BR3-Mediated Processing And Survival (83.2)." Journal of Immunology 178, no. 1_Supplement (2007): S112. http://dx.doi.org/10.4049/jimmunol.178.supp.83.2.

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Abstract Signaling through both the B cell receptor (BCR) and the BLyS receptor, BR3, are required for primary B cell survival. Therefore, understanding how the downstream signaling pathways from these receptors interact should help reveal the molecular mechanisms underlying primary B cell selection and survival. The classical and non-classical NF-kB pathways are an attractive starting point for interrogation, since its members operate downstream of several key B cell signaling systems. Accordingly we have examined BLyS-mediated signaling and survival both in isolation as well as in the contex
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49

Hunter, Zachary R., Xavier Leleu, Daniel D. Santos, et al. "Sequence Analysis in the BLYS and APRIL Receptor TACI Reveals Novel Variants with a Potential Pathogenetic Role in Waldenstrom’s Macroglobulinemia (WM)." Blood 106, no. 11 (2005): 991. http://dx.doi.org/10.1182/blood.v106.11.991.991.

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Abstract B-lymphocyte stimulator protein (BLYS) and a proliferation inducing ligand (APRIL) are members of the tumor necrosis family of ligands which play an important role in normal and malignant human B-cell homeostasis through their receptors BCMA, TACI (for BLYS and APRIL) and BAFF-R (for BLYS only). We previously demonstrated via multicolor flow cytometric and RT-PCR analysis the expression of BLYS and APRIL, along with BCMA, TACI and BAFF-R on lymphoplasmacytic cells (LPC) as well as mast cells, which provide LPC growth support in patients with Waldenstrom’s Macroglobulinemia (WM) (Blood
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50

Chaparro, Alejandra, Víctor Beltrán, Daniel Betancur, et al. "Molecular Biomarkers in Peri-Implant Health and Disease: A Cross-Sectional Pilot Study." International Journal of Molecular Sciences 23, no. 17 (2022): 9802. http://dx.doi.org/10.3390/ijms23179802.

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Background: The aim of this feasibility study was to investigate the concentration level of CCL-20/MIP-3α, BAFF/BLyS, IL-23, RANKL, and Osteoprotegerin in the Peri-Implant Crevicular Fluid (PICF), from patients diagnosed with peri-implant mucositis and peri-implantitis, and to compare them with PICF from patients with healthy implants. Methods: Participants with at least one dental implant with healthy peri-implant tissues, peri-implant mucositis, or peri-implantitis were included. PICF was collected using paper strips from healthy and diseased peri-implant sites (n = 19). Biomarker levels wer
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