Relevant bibliographies by topics / BAFF

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Academic literature on the topic 'BAFF'

Author: Grafiati
Published: 4 June 2021
Last updated: 1 February 2022

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Journal articles on the topic "BAFF"

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Krejsek, Jan, Martina Koláčková, Irena Lindrová, Radovan Slezák, and Ctirad Andrýs. "Increase of Intracellular BAFF in B Cells of Sjögren’s Patients Is Not Affected by Decrease of BAFFR." Acta Medica (Hradec Kralove, Czech Republic) 58, no. 1 (2015): 25–31. http://dx.doi.org/10.14712/18059694.2015.88.

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The presence of a broad spectrum of autoantibodies in Sjögren’s syndrome (SjS) patients is the result of abnormal B-cell regulation that can be at least partially explained by abnormal BAFF/BAFFR regulation. The objective of this study was to determine both membrane and intracellular expression of BAFF/BAFFR in monocytes and B-cells in peripheral blood of 19 primary Sjögren’s syndrome patients and 20 healthy controls using flow cytometry. We also measured sBAFF in serum. Compared to healthy controls, both surface and intracellular expression of BAFF was significantly increased in monocytes and B-cells of SjS patients. Also serum sBAFF level was elevated. Expression of BAFFR on B-cells of SjS patients was surprisingly decreased, but there was no clear increase or decrease within monocytes. Our results indicate that activated monocytes communicate with B-cells via BAFF and BAFFR, so that B-cells are stimulated, but BAFF is also produced to stimulate cells in autocrine way. The decrease of BAFFR expression in SjS patients suggests that there is the mechanism that attempts to take over in order to balance the high level of BAFF.
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Saidoune, F., N. Charles, J. Chezel, B. Escoubet, T. Papo, A. Nicoletti, and K. Sacre. "AB0140 BAFF NEUTRALIZATION HAS JANUS-FACED EFFECT ON ATHEROSCLEROSIS ASSOCIATED WITH SYSTEMIC LUPUS ERYTHEMATOSUS." Annals of the Rheumatic Diseases 79, Suppl 1 (June 2020): 1370.3–1370. http://dx.doi.org/10.1136/annrheumdis-2020-eular.988.

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Background:Cardiovascular diseases (CVD) are the leading cause of death in systemic lupus erythematosus (SLE). B cells play a key role in the pathogenesis of lupus and anti-BAFF therapy has been approved in SLE. Since mature B cells also promote atherosclerosis, BAFF neutralization is expected to have an atheroprotective effect in SLE.Objectives:The aim of our study was to test this hypothesis using a new mouse model with a mix susceptibility to lupus and atherosclerosis that received or not an anti-BAFF treatment, and in a cohort of SLE patients in whom we monitored carotid plaques, the B cell compartment and BAFF levels.Methods:The effect of BAFF on atherosclerosis associated with lupus was investigated in the atherosclerosis- and lupus-proneApoe°D227Kmouse model and in a cohort of SLE patients. Mice were treated with a blocking anti-BAFF monoclonal antibody (Ab), while fed with a standard chow diet. Carotid plaque and carotid intima media thickness were assessed by ultrasound at baseline and during follow-up in SLE patients asymptomatic for CVD.Results:Anti-BAFF Ab inApoe°D227Kmice i/ induced a B cell depletion, ii/ efficiently treated lupus, iii/improved atherosclerosis lesions in mice that had low plasma cholesterol levels but worsened the lesions in mice with high cholesterol levels. In that case, the atheroprotective effect of the BAFF-BAFFR signaling inhibition on B cells was counterbalanced by the proatherogenic effect of the BAFF-TACI signaling inhibition on macrophages. In SLE patients, BAFF blood levels were associated with subclinical atherosclerosis. Anti-BAFF Ab treatment had a differential effect on the intima media thickness progression in SLE patients depending on the body mass indexConclusion:Depending on the balance between metabolic- and B cell-induced proatherogenic conditions, anti-BAFF could be respectively detrimental or beneficial on atherosclerosis development in SLEAcknowledgments:Guillaume Even, Yasmine Lamri, Anh-Thu Gaston,Disclosure of Interests:Fanny Saidoune Grant/research support from: supported by a research partnerships between the academic and GlaxoSmithKline France.Anti-BAFF mAb (IgG1, clone 10F4B) in mice was provided by Glaxosmithkline, Nicolas Charles: None declared, Julie Chezel: None declared, Brigitte Escoubet: None declared, Thomas Papo: None declared, Antonino Nicoletti: None declared, karim sacre: None declared
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Alexaki, Vassilia-Ismini, Vassiliki Pelekanou, George Notas, Maria Venihaki, Marilena Kampa, Valérie Dessirier, Sanaa Sabour-Alaoui, Efstathios N. Stathopoulos, Andreas Tsapis, and Elias Castanas. "B-Cell Maturation Antigen (BCMA) Activation Exerts Specific Proinflammatory Effects in Normal Human Keratinocytes and Is Preferentially Expressed in Inflammatory Skin Pathologies." Endocrinology 153, no. 2 (February 1, 2012): 739–49. http://dx.doi.org/10.1210/en.2011-1504.

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TNFα is known to be expressed in human skin, regulating immune-related responses. Here we report that human normal skin keratinocytes express the members of the TNF superfamily members A proliferation-inducing ligand (APRIL; TNFSF13), B cell-activating factor (BAFF; TNFSF13B), and their receptors, B cell maturation antigen (BCMA; TNFRSF17) and transmembrane activator, calcium-modulator, and cyclophilin ligand interactor (TACI; TNFRSF13B), in a distinct spatial pattern. Our data show a differential expression of these molecules within epidermal layers and skin appendages, whereas the BAFF-specific receptor BAFFR (TNFRSF13C) is absent. Importantly, APRIL and BCMA but not BAFF or TACI are up-regulated in inflammatory skin lesions of psoriasis and squamous cell carcinomas. To explore the functional significance of this system in the skin, we assayed these receptors and ligands in cultured primary keratinocytes and HaCaT cells. We show that both cell types express BAFF, APRIL, BCMA, and TACI. Furthermore, APRIL and/or BAFF trigger nuclear factor-κB activation and IL-6 and granulocyte macrophage colony-stimulating factor (GM-CSF) expression through functional BCMA receptors, an activation inhibited by anti-BCMA short hairpin RNA. However, BAFF and/or APRIL do not induce IL-8 or TNFα production. Our data advance BCMA as an inflammation-related TNFSFR member in keratinocytes, of potential importance in the management of inflammatory skin conditions.
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Xu, Haifeng C., Jun Huang, Vishal Khairnar, Vikas Duhan, Aleksandra A. Pandyra, Melanie Grusdat, Prashant Shinde, et al. "Deficiency of the B Cell-Activating Factor Receptor Results in Limited CD169+Macrophage Function during Viral Infection." Journal of Virology 89, no. 9 (February 11, 2015): 4748–59. http://dx.doi.org/10.1128/jvi.02976-14.

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ABSTRACTThe B cell-activating factor (BAFF) is critical for B cell development and humoral immunity in mice and humans. While the role of BAFF in B cells has been widely described, its role in innate immunity remains unknown. Using BAFF receptor (BAFFR)-deficient mice, we characterized BAFFR-related innate and adaptive immune functions following infection with vesicular stomatitis virus (VSV) and lymphocytic choriomeningitis virus (LCMV). We identified a critical role for BAFFR signaling in the generation and maintenance of the CD169+macrophage compartment. Consequently,Baffr−/−mice exhibited limited induction of innate type I interferon production after viral infection. Lack of BAFFR signaling reduced virus amplification and presentation following viral infection, resulting in highly reduced antiviral adaptive immune responses. As a consequence, BAFFR-deficient mice showed exacerbated and fatal disease after viral infection. Mechanistically, transient lack of B cells inBaffr−/−animals resulted in limited lymphotoxin expression, which is critical for maintenance of CD169+cells. In conclusion, BAFFR signaling affects both innate and adaptive immune activation during viral infections.IMPORTANCEViruses cause acute and chronic infections in humans resulting in millions of deaths every year. Innate immunity is critical for the outcome of a viral infection. Innate type I interferon production can limit viral replication, while adaptive immune priming by innate immune cells induces pathogen-specific immunity with long-term protection. Here, we show that BAFFR deficiency not only perturbed B cells, but also resulted in limited CD169+macrophages. These macrophages are critical in amplifying viral particles to trigger type I interferon production and initiate adaptive immune priming. Consequently, BAFFR deficiency resulted in reduced enforced viral replication, limited type I interferon production, and reduced adaptive immunity compared to BAFFR-competent controls. As a result, BAFFR-deficient mice were predisposed to fatal viral infections. Thus, BAFFR expression is critical for innate immune activation and antiviral immunity.
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Prieto-Peña, D., S. Remuzgo Martinez, F. Genre, V. Pulito-Cueto, B. Atienza-Mateo, B. Sevilla, J. Llorca, et al. "POS0113 BAFF-APRIL-BAFFR PATHWAY ON THE PATHOGENESIS OF IMMUNOGLOBULIN-A VASCULITIS." Annals of the Rheumatic Diseases 80, Suppl 1 (May 19, 2021): 267.2–268. http://dx.doi.org/10.1136/annrheumdis-2021-eular.707.

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Background:BAFF, APRIL and BAFFR are genes that encode cytokines with a key role in the development and survival of B-lymphocytes [1-4]: The B cell-activating factor (BAFF, also known as BLyS), a proliferation-inducing ligand (APRIL) and BAFF receptor (BAFF-R), respectively. Previous genetic studies have revealed that the BAFF-APRIL-BAFFR pathway is implicated in the genetic predisposition to several immune-mediated diseases [5].Objectives:To determine whether the BAFF-APRIL-BAFFR pathway represents a novel genetic risk factor for the pathogenesis of Immunoglobulin-A vasculitis (IgAV), an inflammatory disease in which IgA deposits and B-lymphocytes are crucial [6, 7].Methods:A functional BAFF polymorphism (rs374039502) and two tag variants within APRIL (rs11552708 and rs6608) and BAFFR (rs7290134 and rs77874543) were genotyped in 386 Caucasian IgAV patients (the largest series of Caucasian patients with IgAV ever assessed for genetic studies) and 806 sex and ethnically matched healthy controls by TaqMan assays.Results:No statistically significant differences in the genotype and allele frequencies between patients with IgAV and healthy controls were observed when each genetic variant of BAFF APRIL and BAFFR was analyzed independently (Table 1). Likewise, no statistically significant differences in genotype and allele frequencies of BAFF APRIL or BAFFR were found when patients with IgAV were stratified according to the age at disease onset or to the presence/absence of gastrointestinal or renal manifestations. Similar results were disclosed when haplotype frequencies of APRIL and BAFFR were compared between patients with IgAV and healthy controls as well as patients with IgAV stratified according to the age at disease onset or to the presence/absence of gastrointestinal or renal manifestations.Conclusion:Our results suggest that the BAFF-APRIL-BAFFR pathway does not contribute to the genetic network underlying IgAV.References:[1]J Exp Med 1999;190:1697-710; [2] Science 1999;285:260-3; [3] Nat Genet 2005;37:829-34; [4] Nat Immunol 2002;3:822-9; [5] N Engl J Med 2017;376:1615-26; [6] N Engl J Med 2013;368:2402-14; [7] Autoimmun Rev 2018;17:301-315.Table 1.Genotype and allele frequencies of BAFF, APRIL and BAFFR genes in patients with IgA vasculitis and healthy controls.PolymorphismLocus1/2Data set1/11/22/212rs374039502BAFFT/APatients91.9 (353)8.1 (31)095.9 (737)4.1 (31)Controls91.5 (733)8.1 (65)0.4 (3)95.6 (1531)4.4 (71)rs11552708APRILG/APatients78.1 (299)20.6 (79)1.3 (5)88.4 (677)11.6 (89)Controls77.9 (625)20.4 (1641.6 (13)88.1 (1414)11.9 (190)rs6608APRILC/TPatients71.9 (277)26.0 (100)2.1 (8)84.9 (654)15.1 (116)Controls70.0 (561)27.6 (221)2.5 (20)83.7 (1343)16.3 (261)rs7290134BAFFRA/GPatients58.0 (224)36.3 (140)5.7 (22)76.2 (588)23.8 (184)Controls57.2 (459)36.4 (292)6.5 (52)75.3 (1210)24.6 (396)rs77874543BAFFRG/CPatients82.7 (316)16.0 (61)1.3 (5)90.7 (693)9.3 (71)Controls83.0 (666)16.6 (133)0.4 (3)91.3 (1465)8.7 (139)Acknowledgements:This study was supported by European Union FEDER funds and “Fondo de Investigaciones Sanitarias” (grant PI18/00042) from ‘Instituto de Salud Carlos III’ (ISCIII, Health Ministry, Spain). DP-P is a recipient of a Río Hortega programme fellowship from the ISCIII, co-funded by the European Social Fund (ESF, `Investing in your future´) [grant number CM20/00006]; SR-M is supported by funds of the RETICS Program co-funded by the European Regional Development Fund (ERDF) [grant number RD16/0012/0009]; VP-C is supported by a pre-doctoral grant from IDIVAL [grant number PREVAL 18/01]; BA-M is a recipient of a `López Albo´ Post-Residency Programme funded by Servicio Cántabro de Salud; LL-G is supported by funds of IDIVAL [grant number INNVAL20/06]; RL-M is a recipient of a Miguel Servet type I programme fellowship from the ISCIII, co-funded by the European Social Fund (ESF, `Investing in your future´) [grant number CP16/00033].Disclosure of Interests:Diana Prieto-Peña Speakers bureau: Abbvie, Pfizer, Roche, Bristol-Myers, Janssen and MSD, Consultant of: Abbvie, Pfizer, Roche, Bristol-Myers, Janssen and MSD, Grant/research support from: Abbvie, MSD and Roche, Sara Remuzgo Martinez: None declared, Fernanda Genre: None declared, Verónica Pulito-Cueto: None declared, Belén Atienza-Mateo: None declared, Belén Sevilla: None declared, Javier Llorca: None declared, Norberto Ortego: None declared, Leticia Lera-Gómez: None declared, Maite Leonardo: None declared, Ana Peñalba: None declared, J. Narváez: None declared, Luis Martín-Penagos: None declared, Jose Alberto Miranda-Filloy: None declared, LUIS CAMINAL MONTERO: None declared, PAZ COLLADO: None declared, Javier Sanchez Perez: None declared, Diego de Argila: None declared, Esteban Rubio-Romero: None declared, MANUEL LEON LUQUE: None declared, Juan María Blanco-Madrigal: None declared, E. Galindez: None declared, Javier Martin Ibanez: None declared, Santos Castañeda: None declared, Ricardo Blanco Speakers bureau: Abbvie, Pfizer, Roche, Bristol-Myers, Janssen and MSD, Consultant of: Abbvie, Pfizer, Roche, Bristol-Myers, Janssen and MSD, Grant/research support from: Abbvie, MSD and Roche, Miguel A González-Gay Speakers bureau: Pfizer, Abbvie, MSD, Grant/research support from: Pfizer, Abbvie, MSD, Raquel López-Mejías: None declared
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Bossen, Claudia, Teresa G. Cachero, Aubry Tardivel, Karine Ingold, Laure Willen, Max Dobles, Martin L. Scott, et al. "TACI, unlike BAFF-R, is solely activated by oligomeric BAFF and APRIL to support survival of activated B cells and plasmablasts." Blood 111, no. 3 (February 1, 2008): 1004–12. http://dx.doi.org/10.1182/blood-2007-09-110874.

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Abstract The cytokine BAFF binds to the receptors TACI, BCMA, and BAFF-R on B cells, whereas APRIL binds to TACI and BCMA only. The signaling properties of soluble trimeric BAFF (BAFF 3-mer) were compared with those of higher-order BAFF oligomers. All forms of BAFF bound BAFF-R and TACI, and elicited BAFF-R–dependent signals in primary B cells. In contrast, signaling through TACI in mature B cells or plasmablasts was only achieved by higher-order BAFF and APRIL oligomers, all of which were also po-tent activators of a multimerization-dependent reporter signaling pathway. These results indicate that, although BAFF-R and TACI can provide B cells with similar signals, only BAFF-R, but not TACI, can respond to soluble BAFF 3-mer, which is the main form of BAFF found in circulation. BAFF 60-mer, an efficient TACI agonist, was also detected in plasma of BAFF transgenic and nontransgenic mice and was more than 100-fold more active than BAFF 3-mer for the activation of multimerization-dependent signals. TACI supported survival of activated B cells and plasmablasts in vitro, providing a rational basis to explain the immunoglobulin deficiency reported in TACI-deficient persons.
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Secreto, Frank J., Michelle K. Manske, Tammy Price-Troska, Steven C. Ziesmer, Stephen M. Ansell, James R. Cerhan, and Anne J. Novak. "A Lymphoma-Associated Mutation in BAFF-R Drives Constitutive PI3K Signaling and Increased Expression of Pro-Survival Genes." Blood 118, no. 21 (November 18, 2011): 2642. http://dx.doi.org/10.1182/blood.v118.21.2642.2642.

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Abstract Abstract 2642 BAFF is essential for B cell maturation, and a lack of either BAFF or its primary receptor, BAFF-R, results in a severe depletion of T2 marginal zone and follicular B cells. Elevated serum BAFF levels have been correlated with an increased risk of developing non-Hodgkin's lymphoma (NHL), along with a more aggressive phenotype. A growing body of genetic evidence points toward an association between the development of human disease and variation in genes encoding BAFF and its receptors. Recently, we characterized a novel lymphoma-associated mutation in TNFRSF13C, the gene encoding BAFF-R. This mutation (BAFF-R H159Y) encodes a His159Tyr substitution in the C-terminus of BAFF-R adjacent to the TRAF3 binding motif. Signaling through BAFF-R H159Y results in increased NF-κB activity, elevated immunoglobulin production and increased association with TRAF2, TRAF3 and TRAF6 compared to wild type (WT) BAFF-R. We have detected this mutation in 6% of total NHL cases (n=129), and in 10% of follicular lymphoma (FL) cases (n=41) evaluated thus far. We previously reported that BAFF-R H159Y expressing mouse B cells exhibited significantly more resistance to Fas ligand (FasL) induced apoptosis compared to their cells expressing BAFF-R WT, and we propose here that BAFF-R H159Y mediated increases in PI3K activity may explain such an enhanced anti-apoptotic response. In this study we now show that BAFF stimulated HEK 293 cells stably expressing BAFF-R H159Y not only display significantly increased Akt phosphorylation when compared to BAFF-R WT expressing cells, but also demonstrate robust Akt phosphorylation in the absence of BAFF. BAFF-R H159Y-dependent Akt activation also led to activation of the downstream Akt targets mTOR and GSK3β and their phosphorylation was inhibited following treatment with the PI3- kinase inhibitor wortmannin. We next examined the impact of the BAFF-R H159Y mutation on expression of BAFF-target genes. Quantitative PCR analyses revealed that BAFF-R H159Y cells exhibited a pattern of gene expression indicative of promoting cell survival, displaying significantly higher levels of BCL2, BCL2L1 and PIN1, while down-regulating expression of the pro-apoptotic gene BIM. We recently reported that TRAF6 associates with BAFF-R, and that such binding is more pronounced in cells expressing BAFF-R H159Y. In order to investigate the role TRAF6 plays in mediating BAFF-R-dependent PI3K activity, we silenced TRAF6 expression in HEK 293 and Karpas 422 lymphoma cells using TRAF6 shRNA. Reduced TRAF6 protein expression resulted in a parallel decrease in BAFF-R WT mediated phosphorylation of mTOR in Karpas 422 cells and phosphorylation of both Akt and GSK3β was markedly reduced in BAFF-R H159Y expressing HEK 293 cells. Interestingly, TRAF6 knock-down did not affect NF-kB2 activation in either Karpas 422 or HEK BAFF-R expressing cells suggesting that Akt does not play a role in BAFF-R mediated activation of non-canonical NF-kB. Finally, preliminary co-precipitation studies indicate that Akt can be recruited to BAFF-R itself, and our initial observations suggest that such an association is significantly reduced in cells expressing BAFF-R H159Y. Taken together, these studies suggest that the BAFF-R H159Y mutation confers enhanced BAFF-R-dependent PI3K signaling and pro-survival gene expression independent of BAFF. Moreover, such enhanced P13K activation is partly dependent upon TRAF6, and decreased recruitment of Akt to BAFF-R H159Y may function to increase the amount of this PI3K target for activation. Thus, BAFF-R H159Y likely contributes to BAFF signaling irregularities in NHL patients harboring this mutation, and may predispose individuals to developing lymphoma regardless of their serum BAFF concentration. Disclosures: No relevant conflicts of interest to declare.
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Hildebrand, Joanne M., Zhenghua Luo, Michelle Manske, Steven Ziesmer, Tammy Price-troska, Wai Lin, Bruce Hostager, et al. "A BAFF-R Mutation Associated with Non-Hodgkin Lymphoma Exhibits Altered TRAF Binding and Reveals New Insights Into Proximal BAFF-R Signaling." Blood 116, no. 21 (November 19, 2010): 468. http://dx.doi.org/10.1182/blood.v116.21.468.468.

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Abstract Abstract 468 The requirement for BAFF and BAFF-R in normal human and murine B cells is well studied, but there is also significant evidence to suggest that BAFF plays an important role in malignant B cell proliferation and survival. Serum BAFF levels are elevated in patients with non-Hodgkin lymphoma (NHL) and high BAFF levels correlate with aggressive disease and a poor response to therapy. There is also increasing genetic evidence suggesting an association between the development of human disease and genetic variation in genes encoding BAFF and its receptors. Mutations in TNFRSF13B (TACI) were identified in patients with familial common variable immunodeficiency (CVID) and IgA deficiency and we have found that single nucleotide polymorphisms (SNP) in TNFSF13B (BAFF) are associated with elevated BAFF levels and risk for developing NHL. To build upon these findings we sequenced BAFF and its receptors; TNFSF13B, TNFRSF13B, TNFRSF17(BCMA), and TNFRSF13C (BAFF-R) in NHL patients to identify novel genetic variants that may be associated with NHL risk. Among 40 individual samples (20 controls and 20 follicular lymphoma (FL) cases) that were bi-directionally sequenced we identified a heterozygous cytosine to thymidine transition in 1 patient specimen at position 475 (C475T) of TNFRSF13C. The C475T transition encodes a missense substitution of tyrosine for histidine in codon 159 (H159Y) in the highly conserved cytoplasmic tail of BAFF-R, adjacent to the TRAF3 binding motif PVPAT. We next expanded our analysis of BAFF-R H159Y and analyzed NHL tumor biopsies for the presence of the mutation. 4/41 (10%) follicular lymphomas (FL), 2/42 (5%) diffuse large B cell lymphomas, 1/22 (5%) lymphoplasmacytic lymphomas (LPL), and 1/24 (4%) mucosal associate lymphoid tissue lymphomas carried the heterozygous mutation. The BAFF-R H159Y mutation was not detected in any of the normal control DNA from healthy donors (n=100). Given its close proximity to the TRAF3 binding site in the cytoplasmic domain of BAFF-R we first wanted to determine if the H159Y mutation altered BAFF induced signaling. We generated cell lines that express HA-tagged wildtype BAFF-R, BAFF-R with the H159Y mutation, or BAFF-R with an ablated TRAF3 binding site as a negative control. Analysis of cells expressing H159Y BAFF-R demonstrates that this mutation results in increased BAFF-R-mediated NFκB1 and NF-κB2 activation. The enhanced signal activated by BAFF-R H159Y is coupled with a several fold increase in TRAF3, TRAF2, and TRAF6 recruitment to BAFF-R and increased IgM production. We further demonstrate that recruitment of TRAF6 to BAFF-R is not unique to the mutant H159Y BAFF-R, but is also an important and necessary feature of BAFF-R signaling in normal B cells. Collectively, our data identify a novel lymphoma-associated mutation in BAFF-R and describe exciting new aspects of BAFF-R signaling that are important for understanding normal B cell homeostasis and function, as well as pathogenic BAFF-R contributions to human disease. Disclosures: No relevant conflicts of interest to declare.
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Tada, S., T. Yasui, T. Okuno, Y. Nakatsuji, H. Mochizuki, S. Sakoda, and H. Kikutani. "BAFF controls neural cell survival through BAFF receptor." Journal of the Neurological Sciences 333 (October 2013): e689. http://dx.doi.org/10.1016/j.jns.2013.07.2380.

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Tada, Satoru, Teruhito Yasui, Yuji Nakatsuji, Tatsusada Okuno, Toru Koda, Hideki Mochizuki, Saburo Sakoda, and Hitoshi Kikutani. "BAFF Controls Neural Cell Survival through BAFF Receptor." PLoS ONE 8, no. 7 (July 29, 2013): e70924. http://dx.doi.org/10.1371/journal.pone.0070924.

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Dissertations / Theses on the topic "BAFF"

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Tun, Paul Fei-Tun. "BAFF, B cells and tumour immunity." Thesis, University of Oxford, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.534210.

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Sutherland, Andrew Peter Robert St Vincents Clinical School UNSW. "BAFF regulation of peripheral T cell responses." Awarded by:University of New South Wales. St Vincents Clinical School, 2005. http://handle.unsw.edu.au/1959.4/22788.

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The activation and effector function of CD4+ T cells are critical points of regulation during an antigen specific T cell response. Dysregulation of these processes can lead to the development of human diseases, encompassing both immunodeficiency and autoimmunity. Members of the TNF superfamily have recently emerged as important regulators of T cell responses, with their overexpression causing autoimmune inflammation in animal models. As overproduction of the novel TNF superfamily ligand BAFF is associated with several autoimmune conditions, we sought to examine the potential role of BAFF as a regulator of T cell activation and effector function. We initially demonstrated BAFF costimulation of T cell activation in vitro. Generation of specific monoclonal antibodies identified BAFF-R as the only BAFF receptor present on T cells, and showed that it was expressed in an activation-dependent and subset-specific manner. Impaired BAFF costimulation in BAFF-R deficient mice indicated that BAFF-R was crucial for mediating BAFF effects in T cells. Analysis of T cell responses in vivo revealed that BAFF transgenic mice have increased T cell priming and recall responses to protein antigens, and showed a corresponding increase in the DTH model of Th1 cell-dependent inflammation. In addition, Th2-dependent allergic airway responses are suppressed in BAFF transgenic mice. Crossing to a B cell deficient background revealed that the proinflammatory effects of BAFF on T cell priming and DTH rely on the presence of B cells, while the suppressive effects during allergic airway inflammation are B cell independent. These data demonstrated that BAFF regulated the outcome of T cell responses in vivo and identified BAFF dependent crosstalk between T and B cells. Stimulation of B cells with BAFF induced the upregulation of MHC class II and ICOS-L both in vitro and in vivo. Induction of these cell surface molecules was associated with an increased capacity to induce T cell proliferation, however this effect was independent of ICOS-L expression. Thus it was demonstrated that BAFF regulated T cell activation and effector function both directly, via stimulation of BAFF-R, and indirectly, by altering the function of B cells. These data suggest that BAFF dependent alterations in T cell function may be an additional causative factor in the association between elevated BAFF levels and the generation of autoimmunity.
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Bitoun, Samuel. "Mise au point de modèles animaux pour étudier la physiopathologie de la polyarthrite rhumatoïde et le rôle du méthotrexate dans la tolérisation." Thesis, Université Paris-Saclay (ComUE), 2018. http://www.theses.fr/2018SACLS174.

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La polyarthrite rhumatoïde (PR) est une maladie auto-immune (MAI) dans laquelle des anticorps anti-peptides citrullinés (ACPA) sont un outil diagnostique très spécifique. L’un des traitements clé de la PR est le méthotrexate (MTX). En plus de son action directe sur la maladie il renforce l’effet des anti-TNF alpha (aTNF). Ceci pourrait passer par une prévention de la formation d’anticorps anti-médicaments dirigés contre les aTNF ce qui leur fait perdre leur efficacité.Nous avons développé un modèle macaque pour reproduire la maladie humaine par immunisation avec des peptides citrullinés dans le contexte d’un facteur génétique favorisant la PR : l’épitope HLA partagé. L’immunisation de macaques avec divers peptides citrullinés en utilisant un boost intra-articulaire a déclenché une réponse T et B anti-citrulline et a entraîné une mono-arthrite chronique.Le rôle du MTX sur l’immunogénicité des aTNF a été étudié sur un modèle de souris autoimmunes, les souris BAFF transgéniques (tg) qui présentent une MAI. L’utilisation du MTX juste avant l’injection d’aTNF a permis de prévenir l’immunisation contre ce médicament uniquement chez ces souris BAFFtg et pas chez des souris sauvages ou chez des macaques. Nous avons démontré que ces souris BAFFtg surexprimaient CD73, ce qui permettait une sécrétion accrue d’adénosine et de cellules B régulatrices sous l’effet du MTX. L’interaction entre BAFF et le méthotrexate a été confirmée chez l’homme dans la cohorte ABIRISK : le MTX prévient plus efficacement l’immunogénicité chez les patients avec des taux de BAFF élevés.En conclusion, nous avons mis au point deux nouveaux modèles animaux permettant de mieux comprendre la physiopathologie de la PR et d’optimiser l’utilisation des traitements biologiques qui s’étend dans tous les domaines de la médecine
Title : Development of new animal models to study the pathophysiology of RA and the role of methotrexate-induced tolerance.Keywords : Rheumatoid arthritis, shared epitope, ACPA, immunogenicity, methotrexate, TNF inhibitorsAbstract: Rheumatoid arthritis (RA) is an autoimmune disease (AID) where antibodies directed against citrullinated peptides (ACPA) are highly specific for the diagnosis. One of the key treatments of RA is methotrexate. It has an action on both the disease and reinforces the effect of second line TNF inhibitors (TNFi). MTX might act via prevention of anti-drug antibodies (ADAb) directed against TNFi that are implicated in loss of efficacy of TNFi. We have developed a macaque model to recapitulate the human disease by immunization with citrullinated peptides in the context of a genetic factor favoring RA: the shared epitope on the HLA. Immunization of macaques with citrullinated peptides and intra-articular boost cause an anti-citrulline T and B cell response and a chronic monoarthritis.The role of MTX-induced tolerance against TNFI has been studied in autoimmune BAFF transgenic (tg) mice using MTX just before treatment with TNFi we were able to prevent ADAb formation in BAFFtg mice and not wild type mice or macaques. We identified that BAFFtg mice expressed elevated CD73 leading to more adenosine and regulatory B cells as actors in MTX-induced tolerance. This MTX-BAFF interaction was further confirmed in humans in the ABIRISK cohort where MTX was more efficient to prevent ADAb formation in RA patients with elevated BAFF levels.Setting up two new animal models allows better understanding of RA pathophysiology and better use of biologics that extend to other domains of medicine
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Sellam, Jérémie. "Etude de nouveaux acteurs impliqués dans la physiopathologie du syndrome de Sjögren primaire : Id3, BAFF, BAFF-R et les microparticules circulantes." Paris 11, 2009. http://www.theses.fr/2009PA11T012.

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Groom, Joanna Ruth School of Medicine UNSW. "Loss of immune regulatory checkpoints in BAFF transgenic mice." Awarded by:University of New South Wales. School of Medicine, 2006. http://handle.unsw.edu.au/1959.4/27281.

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Multiple checkpoints control the survival and activation of auto-reactive B cells. The discovery of the TNF family cytokine BAFF has been crucial to understanding peripheral B cell tolerance mechanisms. Homeostatic levels of BAFF are tightly regulated to maintain tolerance in the periphery. Chronically increased levels of BAFF lead to the survival of autoreactive B cells. Autoimmune patients display elevated serum BAFF levels. BAFF Tg mice model this situation with systemically high levels of BAFF and the subsequent development of two separate but related autoimmune syndromes; systemic lupus erythematosus (SLE) and Sj??gren???s syndrome (SS). The work conducted in this thesis further investigates the defects in tolerance down-stream of self-reactive B cell survival, which may contribute to autoimmune disease development in BAFF Tg mice. Expansion of the Marginal zone (MZ) B cell population correlates with the pathogenesis of several models of autoimmune disease. BAFF Tg mice are unique in that they not only display an increased splenic MZ B cell population, but also MZ B cells are found in the salivary glands of mice developing SS. The examination of genes differentially regulated between MZ and Follicular (Fo) B cells led to the investigation of sphingosine-1-phosphate receptor biology. The expression of S1P receptors was shown to be required for the positioning of MZ B cells in the spleen. Chronic BAFF stimulation alters the retention of MZ B cells through the alteration of S1P receptors and decreased integrin activation. The alteration of S1P receptors and increased ligand sensitivity leads to the accumulation of MZ B cells in the inflamed salivary glands of BAFF Tg mice. This works provides a potential mechanism for the tissue specificity seen in systemic autoimmune disease. The provision of T cell help to auto-reactive B cells is thought to underlie the development of SLE. BAFF Tg mice deficient in T cells surprisingly developed an SLE-like disease indistinguishable from that of BAFF Tg mice. Autoimmunity in BAFF Tg mice did however require signals through the toll-like receptor (TLR)-associated signalling adaptor, MyD88, which controlled the production of pathogenic autoantibodies. Therefore, autoimmunity in BAFF Tg mice results from altered B cell tolerance, which requires TLR signalling and is independent of T cell help. It is likely that autoimmune patients with elevated levels of BAFF show a similar basis for disease.
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Murphy, Deirdre. "Investigating the BAFF/APRIL cytokine system in atherosclerosis pathology." Thesis, University of Cambridge, 2015. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.709281.

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Lahiri, Ayan. "The complexity of the BAFF forms and their functional implications." Thesis, Brest, 2014. http://www.theses.fr/2014BRES0006/document.

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BAFF, «facteur d'activation des lymphocytes B (LB) » contribue à l'expansion des LB autoréactifs de faible affinité lors de la mise en place de la tolérance. Cependant, les mécanismes menant à la surexpression de BAFF dans les maladies auto-immunes ne sont pas compris. Nous avons découvert un nouveau variant de BAFF, 4BAFF (dans lequel l'exon 4 est épissé), qui agit comme un facteur de transcription de son propre gène et participe à sa régulation. Ainsi, 4BAFF est préférentiellement observé dans les cellules isolées de patients atteints de maladies auto-immunes. De plus, 4BAFF régule un grand nombre de gènes associés à la réponse immunitaire innée et à la régulation de l’apoptose. Une autre constatation importante est que 4BAFF est un élément clé pour comprendre l’activité des LB régulateurs. Notre travail présente un concept entièrement nouveau suggérant qu'une cytokine peut être régulée par l'activité de l'un de ses variants d'épissage. Par ailleurs, nous avons observé que les cellules épithéliales expriment le récepteur de BAFF : BR3. Le blocage de BR3 se traduit par la translocation nucléaire de PKC et l'apoptose des cellules épithéliales. Par un effet autocrine, nous démontrons que seules certaines formes de BAFF participent à la survie des cellules épithéliales. Enfin , nous avons étudié les conséquences de l'expression du TLR9 à la surface des LB et démontrons que ce TLR9 membranaire ne fixe pas le CpG et agit comme un co-récepteur négatif du BCR. En effet, l'activation des LB par le CpG capté au niveau endosomal, est inhibée par l’action d’un anticorps anti-TLR9 se fixant au niveau membranaire. Tous ces résultats contribuent à une meilleure compréhension des mécanismes impliqués dans l'immunopathologie des maladies autoimmunes avec des applications potentielles en thérapeutique
Elevated expression of ‘B cell activating factor’ (BAFF), a potent B cell survival factor contributes to the expansion of low-affinity self-reactive B cells during the establishment of tolerance. However, mechanisms leading to BAFF over-expression in autoimmune diseases are not understood. We reported the discovery of a new variant for BAFF, 4BAFF in humans (in which exon 4 is excised) or 5BAFF in mice (in which exon 5 is excised), which acts as a transcription factor of the full-length form of BAFF, and which is preferentially found in cells isolated from patients with autoimmune diseases. When transfected in human B cells, D4BAFF upregulates a large number of genes associated with immune response and especially innate immunity and regulation of apoptotis. Furthermore D4BAFF acts, in association with p50 from the NF- B pathway, as a transcription factor for its own parent gene. Another important finding is that 4BAFF is an important component of the efficacy of regulatory B cell activity. Our work introduces an entirely novel concept in biology suggesting that a human cytokine gene can be transcriptionally regulated by the activity of one of its own splice variants.We have also tried to understand the complexity of the various forms of BAFF. We observed that epithelial cells expressed BAFF-receptor (BR3) and produce BAFF suggesting autocrine properties. Blocking BR3 results in nuclear translocation of PKC promoting epithelial cell apoptosis.Furthermore, only some forms of BAFF are required for epithelial cell survival. Finally, we studied the consequences of the expression of TLR9 on the B cell surface and demonstrated that TLR9 acts as a co-receptor of the B cell receptor to influence B cell fate independently of CpG binding. We show that CpG activation of B cells, acting synergistically with BCR signals, was inhibited by anti-TLR9 stimulation. Induction of CD25 expression and proliferation of B cells were thus down-regulated by engagement of cell surface TLR9. Overall, our results indicate that TLR9 expressed on B cell plasma membrane might be a negative regulator of endosomal TLR9, and could provide a novel control by which activation of autoreactive B cells is restrained. All these findings contribute to a better understanding on immunopathology of autoimmune diseases with potential applications in therapy
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Fountain, Kathryn. "The role of the BAFF receptor in B cell survival." Thesis, University College London (University of London), 2017. http://discovery.ucl.ac.uk/10040551/.

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Signalling through the BAFF receptor (BAFFR) is critical for the development and survival of B cells. The binding of BAFF to BAFFR leads to the recruitment and subsequent degradation of TRAF3, which results in the accumulation of NIK and induction of signalling through the non-canonical NFκB pathway. However, recent studies have shown that IKK1, a component of the alternative NFκB pathway, is required for B cell development, but not B cell survival. Concurrently, a number of other signalling molecules were shown to be of importance of B cell survival, including SYK, PI3K and the classical NFκB pathway. However, the mechanisms through which BAFFR transduces signals to these pathways remains unclear. The experiments described in this thesis sought to further understand the role of the BAFFR in controlling B cell survival. I have used inducible deletions to delete BAFFR and TRAF3 in mature B cells to determine their role in B cell survival. I have shown that TRAF3 deletion is only partially able to rescue B cell survival in BAFFR-deficient B cells, suggesting that there are additional interactors of BAFFR that transduce survival signals. To further understand how BAFFR transduces survival signals, I sought to identify novel proteins that interact with BAFFR. I generated a modified tandem affinity purification (moTAP)-BAFF, a tagged version of BAFF that can be used to stimulate and affinity purify BAFFR. Preliminary experiments have shown that, as expected, TRAF3 is one of the most enriched proteins in the BAFFR interactome. BAFF stimulation also leads to the recruitment of CD19 to BAFFR. It is hoped that further analysis of the BAFFR interactome will give insight into the receptor proximal events that control B cell survival. Finally, I developed a B cells survival assay to screen a panel of kinase inhibitors in order to identify novel kinases that are involved in B cell survival.
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Saidoune, Fanny. "Rôle de BAFF dans l'athérome accéléré associé au lupus systémique." Thesis, Université de Paris (2019-....), 2020. http://www.theses.fr/2020UNIP7011.

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Le lupus érythémateux systémique (LES) est une maladie auto-immune caractérisée par des anomalies du système immunitaire inné et adaptatif. Les événements cardiovasculaires sont aujourd’hui la première cause de mortalité des sujets ayant un LES. Ces événements cardiovasculaires, en lien avec l’athérome, sont plus précoces que dans la population générale et ne sont pas complètement expliqués par les facteurs de risque cardiovasculaire classiques. Cet athérome accéléré trouve peut-être une partie de son explication dans l’immunopathogenèse du LES.Les lymphocytes B, par leur capacité à produire des auto-anticorps pathogènes, jouent un rôle causal dans le LES. Les lymphocytes B matures sont dépendants pour leur activation, leur prolifération et leur survie, de la cytokine BAFF. Chez l’homme, le Belimumab (GSK), un anticorps monoclonal spécifiquement dirigé contre BAFF, est la seule biothérapie ayant une AMM en France dans le LES. Le rôle joué par BAFF dans l’athérogenèse est démontré par l’athéroprotection induite par l’invalidation génétique du récepteur de BAFF dans les modèles murins pro-athéromateux. Mon projet de thèse consiste en l’étude de la contribution de BAFF dans l’athérome accéléré associé au lupus.Nous avons tout d’abord montré que, la souris ApoE-/-D227K constituait, contrairement à la souris ApoE-/- pristane, un modèle approprié pour l’étude de l’athérome associé au lupus.Nous avons ensuite montré que, dans le modèle ApoE-/-D227K, la neutralisation de BAFF au moyen d’un anticorps ciblant spécifiquement cette cytokine, traitait efficacement le lupus en induisant la déplétion des lymphocytes B matures au sein des organes lymphoïdes secondaires. En revanche, l’effet athéroprotecteur de la neutralisation de BAFF n’était apparent, malgré la déplétion des lymphocytes B présents au sein des organes lymphoïdes tertiaires aortiques, que pour des taux sériques de cholestérol bas. Pour des taux sériques de cholestérol haut, la neutralisation de BAFF tendait à aggraver les lésions athéromateuses en favorisant la spumification des macrophages exprimant TACI.Nous avons poursuivi nos travaux expérimentaux chez l’humain, en montrant, de façon congruente à ce que nous observions chez la souris, une corrélation positive des taux sériques de BAFF, et de l’expansion périphérique des lymphocytes B avec la progression de la maladie athéromateuse infraclinique chez des patients lupiques à faible risque cardiovasculaire apparent. L’effet du traitement par Belimumab sur l’athérome était également analysé ex vivo et in vitro chez un petit nombre de patients et montrait que la neutralisation de BAFF en contexte lupique pouvait promouvoir ou ralentir le développement de la maladie athéromateuse en fonction de l’indice de masse corporel (IMC).En conclusion, nos travaux montrent 1- que les lymphocytes B matures et BAFF jouent un rôle pathogénique dans l’athérome associé au lupus et 2- que BAFF peut être athéroprotecteur ou athéroaggravant en fonction de la nature des mécanismes impliqués. En l’absence de facteurs de risque cardiovasculaire classiques (dyslipidémie, surpoids), les lymphocytes B jouent un rôle important dans l’athérogenèse associée au lupus et les thérapies neutralisant BAFF, en inhibant l’interaction BAFF/BAFFR sur les lymphocytes B, induisent une déplétion B athéroprotectrice dans les organes lymphoïdes tertiaires. En présence de facteurs de risque cardiovasculaire classiques, les lymphocytes B ne jouent plus qu’un rôle marginal dans l’athérogenèse et les thérapies neutralisant BAFF, en inhibant l’interaction BAFF/TACI sur les macrophages, favorisent la transformation spumeuse athéroaggravante des macrophages
Accelerated atherosclerosis is now recognized as the main cause of death in SLE patients. Of note, the increased prevalence of premature atherosclerosis in SLE is not fully explained by traditional cardiovascular risk factors. Although we and others showed that lupus immunopathogenesis may promote accelerated atherosclerosis, the mechanisms by which SLE pathogenesis might contribute to accelerate atherosclerosis remains elusive.B cells, by their ability to produce pathogenic autoantibodies, play a causative role in SLE. Consistently, there are strong evidence to connect B-cell activating factor (BAFF), a cytokine required for maturation and survival of B2 B cells, to lupus. Belimumab (GSK), a monoclonal antibody specifically directed against BAFF, is the only approved biotherapy for SLE treatment. BAFF is involved in atherosclerosis and atherosclerosis-prone mice in which hematopoietic cells did not express the receptor for the pro-B2 BAFF cytokine displayed a significant reduction in atherosclerotic lesion development. My thesis project consists of studying the contribution of BAFF in accelerated atherosclerosis associated with SLE.We first showed that ApoE-/-D227K mice were an appropriate model for the study of lupus associated atherosclerosis, when compared to the ApoE-/- pristane treated mice.We then demonstrated that, in the ApoE-/-D227K model, the neutralization of BAFF by using an antibody specifically targeting this cytokine, efficiently treated lupus by inducing the depletion of mature B cells in the secondary lymphoid organs. On the other hand, the atheroprotective effect of the BAFF neutralization, despite the depletion of B cells in the aortic tertiary lymphoid organs, was apparent in mice with low cholesterol levels, only. For high cholesterol levels, the neutralization of BAFF tended to aggravate atherosclerotic lesions by promoting the foam cell transformation of macrophages that expressed TACI.We then asked whether the observations made in our mouse model were relevant to human atherosclerosis associated with SLE and observed a positive correlation between BAFF serum levels, peripheral expansion of B lymphocytes and progression of subclinical atherosclerosis in lupus patients at apparent low risk for cardiovascular events. The effect of Belimumab treatment on atherosclerosis was also analyzed ex vivo and in vitro in a small number of patients and we showed that BAFF neutralization in lupus could enhance or dampen the development of atherosclerosis according to the body mass index (BMI).In conclusion, our work shows 1- that B cells and BAFF play a pathogenic role in atherosclerosis associated with lupus and 2-that BAFF can be atheroprotective or atheroaggravative depending on the mechanisms involved. In absence of classical cardiovascular risk factors (such as dysplipidemia or overweight), BAFF neutralizing therapy, by disrupting the BAFF/BAFFR interaction on B cells, depletes mature B cells in tertiary lymphoid organs and is atheroprotective. In the presence of classical cardiovascular risk factors, BAFF neutralizing therapy, by disrupting the BAFF/TACI interaction on macrophages, promotes the foam cell transformation of macrophages and aggravates atherosclerosis
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Chhabra, Manu. "Targeting the BAFF/April signalling axis for prevention of humoral rejection." Thesis, University of Cambridge, 2015. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.708468.

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Books on the topic "BAFF"

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Sateren, Shelley Swanson. Banff. New York: Crestwood House, 1989.

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Barf. Lāhaur: Sang-i Mīl Pablīkeshanz, 2010.

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Jamīlah, Kadīvar, ed. Barf. Tihrān: Umīd-i Īrāniyān, 2004.

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Baffo, Giorgio. giorgio baffo poesie Baffo osceno. Roma: Stampa alternativa, 2001.

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Akbar, Akbar Ḥusain. Barf barf cingārī: Shiʻrī majmūʻah. Kolkata: Raʾīsah Akbar va Munavvar Ḥusain, 2003.

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Hashmi, Saira. Siah baif. Lahore: India-e-Naqush, 1986.

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Thakkar, Anil. Garm barf. Delhi: Modern Books, 1990.

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Ahmad, Razia F. Kālī barf. Lāhaur: Maqbūl Ikāḍamī, 1992.

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Kālī barf. Lāhaur: Maqbūl Ikaiḍamī, 1992.

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Krzyżanowski, Jerzy Ryszard. Banff: Powieść. Paryż: Instytut Literacki, 1988.

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Book chapters on the topic "BAFF"

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Bittenbinder, Elise, Jenny Baron, and Silvia Schriefers. "Eine gewagte Kooperation: BAMF und BAfF." In Grenzbereiche der Supervision - Verwaltung in Bewegung, 65–77. Göttingen: Vandenhoeck & Ruprecht, 2015. http://dx.doi.org/10.13109/9783666403699.65.

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Myles, Arpita, Jean L. Scholz, and Michael P. Cancro. "BAFF/BLyS Family." In Encyclopedia of Signaling Molecules, 523–31. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-67199-4_101556.

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Warnatz, Klaus. "Baff-Receptor Deficiency." In Encyclopedia of Medical Immunology, 1–2. New York, NY: Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4614-9209-2_29-1.

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Smulski, Cristian R., Patricia Odermatt, and Hermann Eibel. "BAFF Receptor Deficiency." In Humoral Primary Immunodeficiencies, 131–47. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-91785-6_11.

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Myles, Arpita, Jean L. Scholz, and Michael P. Cancro. "BAFF/BLyS Family." 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_101556-1.

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Warnatz, Klaus. "Baff-Receptor Deficiency." In Encyclopedia of Medical Immunology, 47–49. New York, NY: Springer New York, 2020. http://dx.doi.org/10.1007/978-1-4614-8678-7_29.

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Davidson, Anne. "BAFF and APRIL and Their Receptors." In Encyclopedia of Medical Immunology, 181–87. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-0-387-84828-0_563.

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Mackay, Fabienne, William A. Figgett, Pali Verma, and Xavier Mariette. "The BAFF/APRIL System in Autoimmunity." In BLyS Ligands and Receptors, 125–60. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-60327-013-7_7.

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Hildebrand, Joanne M., Ping Xie, and Gail A. Bishop. "Signal Transduction by Receptors for BAFF and APRIL." In BLyS Ligands and Receptors, 93–114. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-60327-013-7_5.

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Ryan, Maureen C., and Iqbal S. Grewal. "Targeting of BAFF and APRIL for Autoimmunity and Oncology." In Advances in Experimental Medicine and Biology, 52–63. New York, NY: Springer New York, 2009. http://dx.doi.org/10.1007/978-0-387-89520-8_4.

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Conference papers on the topic "BAFF"

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Al-Fatlawi, Noor Alhuda Ghanem, Arshad N. G. Al-Dujaili, and Talib Hussein Nooruldeen Kammona. "Assessment B-cell-activating factor (BAFF) in thrombocytopenia patients." In INTERNATIONAL CONFERENCE OF NUMERICAL ANALYSIS AND APPLIED MATHEMATICS ICNAAM 2019. AIP Publishing, 2020. http://dx.doi.org/10.1063/5.0027533.

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Samuel, Du, Jacobs Holly M, Arkatkar Tanvi, Scharping Nicole, Rawlings David J, and Jackson Shaun W. "AI-16 Integration of BCR, TLR, BAFF receptor and TACI signals promotes autoantibody production by transitional B cells in BAFF transgenic mice." In LUPUS 21ST CENTURY 2018 CONFERENCE, Abstracts of the Fourth Biannual Scientific Meeting of the North and South American and Caribbean Lupus Community, Armonk, New York, USA, September 13 – 15, 2018. Lupus Foundation of America, 2018. http://dx.doi.org/10.1136/lupus-2018-lsm.16.

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Jha, Saket, Jagdeep Singh, Ranjana Minz, Aadhar Dhooria, Gsrsnk Naidu, Rajiv Kumar, Manish Rathi, Sanjay Jain, Shashi Anand, and Aman Sharma. "FRI0280 BAFF AND APRIL GENE EXPRESSION IN PATIENTS WITH ANCA ASSOCIATED VASCULITIS." In Annual European Congress of Rheumatology, EULAR 2019, Madrid, 12–15 June 2019. BMJ Publishing Group Ltd and European League Against Rheumatism, 2019. http://dx.doi.org/10.1136/annrheumdis-2019-eular.2217.

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Hsu, H., M. Zhang, K. Miner, G. Kevin, J. Whoriskey, R. Jacobsen, C. Chen, and K. Ishida. "FRI0306 Development of baff and icosl bispecific inhibitor amg 570 for sle treatment." In Annual European Congress of Rheumatology, EULAR 2018, Amsterdam, 13–16 June 2018. BMJ Publishing Group Ltd and European League Against Rheumatism, 2018. http://dx.doi.org/10.1136/annrheumdis-2018-eular.5767.

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Figgett, W., A. Baldolli, F. Vincent, and F. Mackay. "36 Identification of disease-associated gut microbiota in lupus-prone baff-tg mice." In LUPUS 2017 & ACA 2017, (12th International Congress on SLE &, 7th Asian Congress on Autoimmunity). Lupus Foundation of America, 2017. http://dx.doi.org/10.1136/lupus-2017-000215.36.

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Polverino, F., S. Baraldo, E. Bazzan, G. Turato, S. Agostini, E. Balestro, M. Damin, et al. "B Cell Activating Factor (BAFF) Is Expressed by Lymphoid Follicles of COPD Patients." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a2951.

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Campos, J., T. Slocombe, S. Nayar, V. Iannizzotto, DH Gardner, CD Buckley, A. Haynes, RB Henderson, and F. Barone. "P061 Targeting B-cell activating factor (BAFF) impairs ectopic lymphoneogenesis in murine models of sjÖgren’s syndrome." In 38th European Workshop for Rheumatology Research, 22–24 February 2018, Geneva, Switzerland. BMJ Publishing Group Ltd and European League Against Rheumatism, 2018. http://dx.doi.org/10.1136/annrheumdis-2018-ewrr2018.80.

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Alfano, Gianvincenzo, Sergio Greco, Francesco Parisi, and Irina Trubitsyna. "Defining the Semantics of Abstract Argumentation Frameworks through Logic Programs and Partial Stable Models (Extended Abstract)." In Thirtieth International Joint Conference on Artificial Intelligence {IJCAI-21}. California: International Joint Conferences on Artificial Intelligence Organization, 2021. http://dx.doi.org/10.24963/ijcai.2021/641.

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Extensions of Dung’s Argumentation Framework (AF) include the class of Recursive Bipolar AFs (Rec-BAFs), i.e. AFs with recursive attacks and supports. We show that a Rec-BAF \Delta can be translated into a logic program P_\Delta so that the extensions of \Delta under different semantics coincide with subsets of the partial stable models of P_\Delta.
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Flessa, Christina Maria, Adrianos Nezos, Evangelia Zampeli, Haralampos M. Moutsopoulos, and Clio Mavragani. "AB0181 ASSOCIATION BETWEEN SINGLE NUCLEOTIDE POLYMORPHISMS (SNPS) OF THE BAFF GENE AND FATIGUE IN PRIMARY SJöGREN’S SYNDROME." In Annual European Congress of Rheumatology, EULAR 2019, Madrid, 12–15 June 2019. BMJ Publishing Group Ltd and European League Against Rheumatism, 2019. http://dx.doi.org/10.1136/annrheumdis-2019-eular.7024.

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Parodis, I., F. Söder, F. Faustini, Z. Kasza, F. Wermeling, and I. Gunnarsson. "PS7:134 Rituximab-mediated late-onset neutropenia in systemic lupus erythematosus – distinct roles of baff and april." In 11th European Lupus Meeting, Düsseldorf, Germany, 21–24 March 2018, Abstract presentations. Lupus Foundation of America, 2018. http://dx.doi.org/10.1136/lupus-2018-abstract.177.

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Reports on the topic "BAFF"

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Dutra, Jose. OERDifferentiation Presentation April Banff Canana. NPT Educacional, March 2015. http://dx.doi.org/10.17699/ind.2015.2.

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Couture, R., and S. G. Evans. Five-Mile Creek debris flow, Banff National Park, near Banff, Alberta, August 4, 1999. Natural Resources Canada/ESS/Scientific and Technical Publishing Services, 2000. http://dx.doi.org/10.4095/211547.

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Yeo, W. B. When Banff was somewhere else down the track. Natural Resources Canada/ESS/Scientific and Technical Publishing Services, 1985. http://dx.doi.org/10.4095/298182.

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Jordan, Tyler. Development of an ultra-fast BaF2-based detector. Office of Scientific and Technical Information (OSTI), November 2020. http://dx.doi.org/10.2172/1726114.

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Carter, J. L. Lower carboniferous brachiopods from the Banff formation of western Alberta. Natural Resources Canada/ESS/Scientific and Technical Publishing Services, 1987. http://dx.doi.org/10.4095/122462.

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Lourenço-Leitzke, Milene Rocha, and Marlene Marchiori. Comunicação de Risco: um descompasso entre discurso e prática no caso Shell/Basf / Risk Communication: Mismatch between speech and practice in Shell/Basf case. Revista Internacional de Relaciones Públicas, December 2016. http://dx.doi.org/10.5783/rirp-12-2016-07-107-124.

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Medioli, B. E., and M. N. Demuth. Reconnaissance sub-bottom profiling studies of Peyto Lake, Banff National Park. Natural Resources Canada/ESS/Scientific and Technical Publishing Services, 2009. http://dx.doi.org/10.4095/247448.

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Medioli, B. E., and M. N. Demuth. Sub-bottom profiling results from Peyto Lake, Banff National Park, Alberta. Natural Resources Canada/ESS/Scientific and Technical Publishing Services, 2009. http://dx.doi.org/10.4095/247419.

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Gardner C., L. Ahrens, J. W. Glenn, J. A. Kozak, and J. F. Ryan. Booster Fault Study for the BAF Penetration Site. Office of Scientific and Technical Information (OSTI), January 2000. http://dx.doi.org/10.2172/1132453.

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Jordan, Tyler Alexander. Development of an ultra-fast BaF₂-based detector. Office of Scientific and Technical Information (OSTI), April 2020. http://dx.doi.org/10.2172/1615640.

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