B cell-activating factor belonging to the TNF family (BAFF) and its receptor BAFF-R play critical roles in the maturation and survival of conventional peripheral B cells. However, they appeared to be dispensable for the generation and maintenance of CD5(+) B-1 cells as BAFF(-/-) and BAFF-R(-/-) mice have normal B-1 cell populations. Hence, it is presently unclear if B-1 cells are responsive to BAFF and if BAFF regulates some aspects of B-1 cell function. We show here that BAFF-R and transmembrane activator and CAML interactor (TACI) are the major receptors expressed by B-1 cells. Specifically, we show that BAFF treatment of B-1 cells leads to increased NF-kappaB p100 processing and CD21/CD35 expression. Interestingly, toll-like receptor (TLR) engagement of B-1 cells augmented the surface expression of BAFF receptors and rendered them responsive to BAFF costimulation, as evidenced by their increased proliferation, expression of cell surface activation markers and secretion of the pro-inflammatory

Introduction Blisibimod is a potent B cell-activating aspect (BAFF) antagonist that binds to both cell membrane-expressed and soluble BAFF. B cells reverted to baseline, resulting in a calculated 30 percent30 % decrease in total B cells by around 160 days following the 1st dosage. In both solitary- and multiple-dosing SC cohorts, the pharmacokinetic profile indicated sluggish absorption, dose-proportional publicity from 0.3 through 3.0 mg/kg SC and 1 through 6 mg/kg IV, linear pharmacokinetics over the dosage selection of 1.0C6.0 mg/kg, and accumulation ratios which range from 2.21 to 2.76. The comparative increase in memory space B cells had not been associated with security signals, as well as the 1192500-31-4 supplier occurrence of adverse occasions, anti-blisibimod antibodies, and medical laboratory abnormalities had been similar between blisibimod- and placebo-treated topics. Conclusions Blisibimod transformed the constituency from the B cell pool and solitary and multiple dosages of ...

Naive peripheral B cells survive in vivo because of active stimulation by the TNF superfamily ligand B lymphocyte stimulator (BLyS/BAFF). Although the survival promoting properties of BLyS are well known, the signal pathways and molecular effectors that characterize this stimulation are still being elucidated. In this communication, we discuss the signal cascades that effect BLyS dependent survival and the regulation of BLyS induced signaling. We also examine the role of BLyS as a growth factor and propose that BLyS induced metabolic enhancement optimizes the B cell response to BCR and TLR-dependent signaling.

Measure human BAFF/BLyS in cell culture supernates, serum, and plasma with our highly sensitive BAFF/BLyS/TNFSF13B Quantikine ELISA Kit.

BAFF belongs to the tumor necrosis factor (TNF) family, and its downstream signaling plays a critical role in B-cell survival and maturation.

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TY - JOUR. T1 - BAFF expression correlates with idiopathic inflammatory myopathy disease activity measures and autoantibodies. AU - López De Padilla, Consuelo M.. AU - McNallan, Kelly T.. AU - Crowson, Cynthia S.. AU - Bilgic, Hatice. AU - Bram, Richard J.. AU - Hein, Molly S.. AU - Ytterberg, Steven R.. AU - Amin, Shreyasee. AU - Peterson, Erik J.. AU - Baechler, Emily C.. AU - Reed, Ann M.. PY - 2013/3/1. Y1 - 2013/3/1. N2 - Objective. To investigate B cell survival cytokine messenger RNA (mRNA) levels as biomarkers of idiopathic inflammatory myopathies (IIM). Methods. We measured and compared mRNA levels of B cell survival cytokines by quantitative real-time polymerase chain reaction in 98 patients with IIM, 38 patients with systemic lupus erythematosus, and 21 healthy controls. The cytokines were B cell-activating factor belonging to the tumor necrosis factor family (BAFF);ΔBAFF; and a proliferation-inducing ligand (APRIL); and their receptors BAFF-R, transmembrane activator and calcium ...

Abstract: Autoimmunity is traditionally attributed to altered lymphoid cell selection and/or tolerance, whereas the contribution of innate immune cells is less well understood. Autoimmunity is also associated with increased levels of B cell-activating factor of the TNF family (BAFF; also known as B lymphocyte stimulator), a cytokine that promotes survival of self-reactive B cell clones. We describe an important role for myeloid cells in autoimmune disease progression. Using Lyn-deficient mice, we show that overproduction of BAFF by hyperactive myeloid cells contributes to inflammation and autoimmunity in part by acting directly on T cells to induce the release of IFN-. Genetic deletion of IFN- or reduction of BAFF activity, achieved by either reducing myeloid cell hyperproduction or by treating with an anti-BAFF monoclonal antibody, reduced disease development in lyn-/- mice. The increased production of IFN- in lyn-/- mice feeds back on the myeloid cells to further stimulate BAFF release. ...

Mice were rendered specifically tolerant to the fluorescein isothiocyanatedextran (FITC) epitope by injection of FITC-dextran B512. Their spleen cells were removed at various times and cultivated in vitro with different polyclonal B-cell activators, such as lipopolysaccharide (LPS), purified protein derivative of tuberculin, and native dextran. LPS caused the appearance of high affinity anti-FITC plaque-forming cells to an equal extent with cells from untreated and tolerant animals, whereas native dextran failed to activate cells from tolerant mice, although it was a potent activator of normal cells. It was concluded that tolerance induction only affects those B cells that could respond to the polyclonal B-cell-activating properties of the tolerogen, but not other B cells having an identical set of Ig receptors directed against the tolerogen. ...

Results The mean disease duration of SLE was 7,0 [2,0-10,0] years, SLEDAI 2K score - 4 [2-13], SLICC damage index score - 0 [0-1], current prednisone dose - 10,0 [7,5-25,0] mg/day. SLE pts did not differ from healthy controls in BAFF (0,02 [0,02-0,08] vs 0,02 [0,02-0,02] ng/ml) and APRIL (0,01 [0,01-0,62] vs 0,01 [0,01-0,01] ng/ml) levels. Among SLE pts BAFF level correlated with lupus anticoagulant (r=0,88, p,0,05) and ESR (r=0,43, p,0,05); APRIL level correlated with SLEDAI 2K (r=0,55, p,0,01), CRP (r=0,50, p,0,01), antiDNA (r=0,38, p,0,05), creatinine level (r=0,39, p,0,05), current prednisone dose (r=0,55, p,0,01) and CD19 B lymphocytes absolute count (r=0,89, p,0,05). We divided SLE pts on two groups: the 1st- pts with high activity (SLEDAI 2K≥8), the 2nd - pts with low (SLEDAI 2K,8). The patients of 1st group had higher level of APRIL (1,69 [0,01-4,0] vs 0,01 [0,01-0,01] ng/ml, p,0,05) compared to 2nd group and control, there is no difference in BAFF level in these groups.. ...

In B cells Uniquely, deletion from the adaptor proteins TRAF3 (TNF receptor-associated factor 3) causes enhanced survival; TRAF3 insufficiency is normally observed in a considerable percentage of individual B-cell malignancies. to harbor mutations (5, 6). Lesions in individual genes may also be observed in Hodgkins lymphoma (7) and connected with particular chromosome 14 deletions in a variety of B-cell lymphomas (8). Oddly enough, mutations will also be common in canine B-cell lymphomas (5). TRAF3 is definitely a negative regulator Impurity C of Alfacalcidol of the noncanonical NF-B (NF-B2) pathway, and enhanced survival in TRAF3-deficient B cells is definitely associated with constitutive activation of NF-B2 (2, 9). BAFF binds to BAFF receptor (BAFFR) to activate a complex signaling cascade that includes TRAF3 degradation and NF-B2 activation, ultimately promoting B-cell survival (10, 11). However, NF-B2 activation is not sufficient to promote enhanced survival, because TRAF3-deficient T cells ...

The samples used in this paper were obtained from patients with osteoarthritis (OA) or RA during knee-TEP operations. First of all, expression of the known BAFF-binding receptors BCMA, TACI and BAFF-R was analyzed in SF of patients with OA and RA using flow cytometry and immunohistochemistry. In a further step, the influence of several stimulants, including cytokines, TLR-agonists and cell activators on receptor expression was tested. Finally, taking into account BAFF function in other cell types, SF were stimulated with BAFF and stained with Annexin V in order to analyze its effect on apoptosis in SF ...

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Objective: To assess the effects of tumour necrosis factor (TNF) antagonist therapy on B lymphocyte stimulator (BLyS) expression in patients with rheumatoid arthritis (RA).. Methods: Blood from 38 patients with RA from a single centre was collected prior to and following initiation of TNF antagonist therapy. Plasma BLyS protein levels, blood leukocyte BLyS mRNA levels and disease activity were longitudinally monitored. Twelve patients with RA who either refused or were felt not to be candidates for TNF antagonist therapy and five normal healthy volunteers served as TNF antagonist-naïve controls.. Results: Baseline plasma BLyS protein levels, but not blood leukocyte BLyS mRNA levels, were elevated in patients with RA. Plasma BLyS protein levels declined following initiation of TNF antagonist therapy in good responders (GR) to TNF antagonist therapy but not in poor responders (PR). By contrast, the erythrocyte sedimentation rate (ESR) declined in response to TNF antagonist therapy in GR and PR. ...

A tumor necrosis factor superfamily member that plays a role in the regulation of B-LYMPHOCYTE survival. It occurs as a membrane-bound protein that is cleaved to release an biologically active soluble form with specificity to TRANSMEMBRANE ACTIVATOR AND CAML INTERACTOR PROTEIN; B-CELL ACTIVATION FACTOR RECEPTOR; and B-CELL MATURATION ANTIGEN ...

In our previous study, overexpression of extracellular proteinase inhibitor (Expi) gene accelerated apoptosis of mammary epithelial cells, and induced expression of B cell activating factor (BAFF) gene. In this study, we found induction of BAFF-receptor (BAFF-R) gene expression in the Expi-transfected cells. A proliferation-inducing ligand (APRIL) gene is another TNF family member and the closest known relative of BAFF. We found induction of APRIL gene expression in the Expi-overexpressed apoptotic cells. NF-B gene was also induced in the Expi-overexpressed cells. Expression patterns of BAFF and APRIL pathway-related genes were examined in in vivo mouse mammary gland at various reproductive stages. Expression levels of BAFF gene were very low at early pregnancy, increased from mid-pregnancy, and peaked at lactation, and thereafter decreased at involution stages of mammary gland. Expression of BAFF-R gene was highly induced in involution stages compared to lactation stages. Thus, expression ...

Background B cell activating factor (BAFF) plays an important role in the differentiation, survival and activation of B cells rheumatoid arthritis (RA). BAFF receptor (BAFFR) is a crucial receptor for the survival of mature B cells in developing B cells. Paeoniflorin-6-O-benzene sulfonate (CP-25) exerted its anti-inflammatory effects through regulating immune cells responses. The study was to investigate the regulatory effect of CP-25 on BAFF/BAFFR-nuclear factor of kappa B (NFkapaB) signaling in B cell of collagen induced-arthritis (CIA) mice.Methods Mice CIA was induced by injection of type II collagen. Arthritis index (AI) and swollen joint count (SJC) were assessed, spleen and joints histopathology were observed.B cells subsets, BAFF receptor were analyzed by flow cytometry. BAFF and immunoglobulin (Ig) levels were measured by protein antibody array. The expressions of TRAF2, MKK3, MKK6, p-P38, and p-NFkapaB65 in NF-kapaB signaling were analyzed by western blot ...

The autoimmune exocrinopathy Sjögrens syndrome (SS) is characterized by mononuclear cell (MNC) infiltrates of exocrine glands and overactivity of B lymphocytes. Although T cells have long been perceived as the prime effectors, increasing evidence indicates that the key role is rather served by B cells. Among related abnormalities are rheumatoid factor (RF), anti-SSA/Ro, and anti-SSB/La antibodies (Ab). Also, supporting this view is our finding of an increase in the number of circulating naïve mature B (Bm) cells, with a reciprocal decrease in that of memory B cells. Furthermore, a ratio of Bm2-plus-Bm2 cells to early Bm5-plus-late Bm5 above 5 is diagnostic. This variation partly reflects the migration of active memory B cells into the exocrine glands of the patients, as well as into their skin. More recently, the B-cell-activating factor of the TNF family (BAFF) has been endorsed with a pivotal role in B-cell survival and hence implicated in the pathogenesis of autoimmunity. In practice, B cells

The tumor necrosis family member BAFF is limiting for the survival of follicular B lymphocytes, but excessive BAFF signaling can lead to autoimmunity, suggesting that its activity must be tightly regulated. We have identified a conserved alternate splice isoform of BAFF, called deltaBAFF, which lacks 57 nt encoding the A-A1 loop and is co-expressed with BAFF in many mouse and human myeloid cells. Mouse deltaBAFF appears on the plasma membrane, but unlike BAFF it is inefficiently released by proteolysis. DeltaBAFF can associate with BAFF in heteromultimers and diminish BAFF bioactivity and release. Thus, alternative splicing of the BAFF gene suppresses BAFF B cell stimulatory function in several ways, and deltaBAFF may promote other functions as well ...

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 transitional, follicular, and marginal zone pools which persist for ~40 days. In contrast, the only bone marrow subset affected is the mature recirculating B cell fraction. Interestingly, splenic B1 cells, but not peritoneal B1 cells, are reduced as well. Following the recovery of serum BLyS levels, peripheral reconstitution occurs gradually, such that normal B cell numbers return by day 70-80. Mice challenged with ...

Belimumab (also known as Benlysta™) is currently being studied in Phase III clinical trials to determine whether or not it is effective for lupus. Belimumab specifically reduces the actions of a protein called B lymphocyte stimulator, or BLyS. BLyS is a protein that increases the lifespan and inflammatory potential of certain immune cells called B cells, which are known to be hyperactive in lupus patients. Belimumab, which interferes with BLyS, is a human antibody. This means that it looks a lot like the antibodies that the immune system makes to fight off viruses. But in this case, belimumab targets only the protein BLyS. Because it only has one target, it is called a monoclonal antibody ...

D to neuronal cultures. Blocking BAFF-R ligation with TACI-Ig inhibited wild-type, but not Baffrm/m, neuronal survival in a dose-dependent manner (Fig. 3 C).

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B-cell activating factor (BAFF), also known as BlyS, TALL-1, TNAK, and zTNF4, is a TNF ligand superfamily member and has been designated TNFSF13B. It is produced by macrophages, dendritic cells, and T lymphocytes. BAFF promotes the survival of B cells and is essential for B cell maturation (1‑4). BAFF binds to three TNF receptor superfamily members: B‑cell maturation antigen (BCMA/TNFRSF17), transmembrane activator and calcium-modulator and cyclophilin ligand interactor (TACI/TNFRSF13B) and BAFF receptor (BAFF R/BR3/TNFRSF 13C). These receptors are type III transmembrane proteins that lack a signal peptide. Whereas TACI and BCMA bind BAFF and another TNF superfamily ligand, APRIL(a proliferation-inducing ligand), BAFF-R selectively binds BAFF. Mouse BAFF-R cDNA encodes a 175 amino acid residue (aa) transmembrane protein with a 71 aa extracellular domain, a 21 aa transmembrane domain, and a 83 aa cytoplasmic region. A second isoform of BAFF R that has a 72 aa cytoplamic region can also be ...

Circulating endothelial progenitor cells (EPCs) are biologic markers of endothelial function. In patients with systemic lupus erythematosus (SLE), the numerical reduction and functional impairment of EPCs contribute to the endothelial dysfunction. Through ex vivo and in vitro studies, we aimed at evaluating the effects of B lymphocyte stimulator (BLyS) on EPC colonies and endothelial cells and also investigating BLyS receptor expression on these cells. EPCs were isolated from peripheral blood mononuclear cells (PBMC). In order to evaluate their ability to form colonies, EPCs were cultured on fibronectin-coated dishes and incubated with BlyS alone or BlyS and belimumab. Apoptosis of EPCs and endothelial cell line EA.hy926 was evaluated after 6, 12, and 24 h of incubation with BLyS and after 6 h with BLyS and belimumab. The expression of B cell activating factor-receptor (BAFF-R), B cell maturation antigen (BCMA), and transmembrane activator and calcium modulator and cyclophilin ligand (CAML) interactor

A Tumor Necrosis Factor superfamily member that plays a Role in the Regulation of B-Lymphocyte Survival. It occurs as a Membrane-bound protein that is cleaved to release an biologically active soluble form with specificity to Transmembrane Activator and CAML Interactor Protein; B-Cell Activation Factor Receptor; and B-Cell Maturation Antigen ...

Toda la información sobre las últimas publicaciones científicas de la Clínica Universidad de Navarra. Increased expression of A Proliferation-inducing Ligand (APRIL) in lung leukocytes and alveolar epithelial cells in COPD patients with non small cell lung cancer

Clinical hypertension is associated with raised serum IgG antibodies. However, whether antibodies are causative agents in hypertension remains unknown. We investigated whether hypertension in mice is associated with B-cell activation and IgG production and moreover whether B-cell/IgG deficiency affords protection against hypertension and vascular remodeling. Angiotensin II (Ang II) infusion (0.7 mg/kg per day; 28 days) was associated with (1) a 25% increase in the proportion of splenic B cells expressing the activation marker CD86, (2) an 80% increase in splenic plasma cell numbers, (3) a 500% increase in circulating IgG, and (4) marked IgG accumulation in the aortic adventitia. In B-cell-activating factor receptor-deficient (BAFF-R−/−) mice, which lack mature B cells, there was no evidence of Ang II-induced increases in serum IgG. Furthermore, the hypertensive response to Ang II was attenuated in BAFF-R−/− (Δ30±4 mm Hg) relative to wild-type (Δ41±5 mm Hg) mice, and this response was ...

Cytokine that binds to TNFRSF13B/TACI and TNFRSF17/BCMA. TNFSF13/APRIL binds to the same 2 receptors. Together, they form a 2 ligands -2 receptors pathway involved in the stimulation of B- and T-cell function and the regulation of humoral immunity. A third B-cell specific BAFF-receptor (BAFFR/BR3) promotes the survival of mature B-cells and the B-cell response.

The indolent B-cell malignancies of lymphoma and myeloma account for a great number of adult cancers in the United States annually. Hi-dose combination chemotherapy, bone marrow transplants and monoclonal antibody therapeutics have improved the clinical responses of patients diagnosed with some of these deadly diseases, but relapses are common. Active immunotherapy of B-cell malignancies is an important and under-exploited field of cancer treatments that may serve to generate potent anti-tumor immunity with long-term anti-tumor memory and surveillance, given the appropriate vaccine intervention approach. We have leveraged the synergistic pairing of agonistic_CD40 monoclonal antibody with the Toll-Like Receptor (TLR)-7 agonist S27609 in therapeutic protection and cellular studies in mouse models of lymphoma and multiple myeloma. In addition, we have explored BAFF/APRIL survival factor blockade in a mouse model of multiple myeloma through the use of soluble BAFF-Receptor and TACI. The studies ...

We show here that approximately 25% of the mature peripheral B cells can survive in the mouse for at least 2 months without Syk, in a manner that requires BAFF‐R and CD19 signaling. In contrast, deletion of the Syk gene in early B cells results in the appearance of a small number of immature IgM+ B cells, which, however, fail to give rise to any mature B cells in the periphery (Cheng et al, 1995). Thus, pre‐B and mature B cells have different requirements for Syk. Indeed, the pre‐BCR is an autonomously signaling receptor that continuously engages Syk, whereas the BCR forms an autoinhibited oligomer on mature B cells that is not in contact with Syk. This notion is supported by a proximity ligation analysis showing that Syk is localized near the BCR only after BCR activation (Infantino et al, 2010; Klasener et al, 2014).. The presence of large amounts of Syk‐negative mature B cells in the induced mb1‐CreERT2;Sykfl/fl mice allowed us to analyze the in vivo role of this kinase in the ...

We show here that approximately 25% of the mature peripheral B cells can survive in the mouse for at least 2 months without Syk, in a manner that requires BAFF‐R and CD19 signaling. In contrast, deletion of the Syk gene in early B cells results in the appearance of a small number of immature IgM+ B cells, which, however, fail to give rise to any mature B cells in the periphery (Cheng et al, 1995). Thus, pre‐B and mature B cells have different requirements for Syk. Indeed, the pre‐BCR is an autonomously signaling receptor that continuously engages Syk, whereas the BCR forms an autoinhibited oligomer on mature B cells that is not in contact with Syk. This notion is supported by a proximity ligation analysis showing that Syk is localized near the BCR only after BCR activation (Infantino et al, 2010; Klasener et al, 2014).. The presence of large amounts of Syk‐negative mature B cells in the induced mb1‐CreERT2;Sykfl/fl mice allowed us to analyze the in vivo role of this kinase in the ...

CD180 (RP105), expressed on dendritic cells and B cells, is a receptor closely related to TLR4. CD180 signaling does not require adaptor proteins like MyD88, instead it resembles B cell receptor (BCR) signaling, including the activation of PI3K and Akt. Recently, others and we have found αCD180 also induces the Pim-1 kinase, but much of the CD180 signaling pathway remains ill defined. We previously found that targeting antigen (Ag) to B cells via CD180, by coupling the Ag to an anti-CD180 antibody (Ag-αCD180), induces a rapid and strong Ag-specific IgG antibody (Ab) response in mice. Furthermore, IgG Ab responses were maintained in immunodeficient mice that lack mature B cells (BAFFR−/−). These studies led us to investigate the signaling events that occur within B cells upon coincident activation of the BCR and CD180. For this study we have employed B1-8hi transgenic mice, which have a BCR that binds to NP-hapten on some splenic B cells, and the K46μm17 murine B cell line, that expresses ...

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A Proliferation Inducing Ligand (APRIL) is a TNF ligand that, via its receptors TACI and BCMA, is involved in both B cell physiology as well as in proliferation and survival of malignant B cells. To target APRIL-dependent stimulation of B cell cancers, we recently produced and characterized two monoclonal antagonistic anti-human APRIL antibodies called humanAPRIL.01A (hA.01A) and humanAPRIL.03A (hA.03A). In a first biochemical assay to validate their blocking activity, hA.01A was shown to fully prevent APRIL from binding to its receptors, whereas a substantial difference was detected for hA.03A, which inhibited APRIL binding to BCMA less efficiently than hA.01A. Epitope mapping subsequently revealed that hA.01A and hA.03A bind distinct sites on APRIL, which provided a structural rationale of their different blocking activities. Importantly, this differential inhibition profile can be used to functionally dissect BCMA and TACI-dependent signals and indicated that B cell survival and IgA ...

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BLyS Human Recombinant fused to His tag at N-terminus produced in E.Coli is a single, non-glycosylated polypeptide chain containing 190 amino acids and having a molecular mass of 21 kDa.

Hyperactive secretion and pathogenic effects of interleukin (IL)-17 and IgA have been detected in different arthropathies. Recent evidence has revealed that TH17 cytokines regulate mucosal IgA secretion. However, it is unknown whether and how IL-17 mediates synovial IgA production. Here we aim to investigate the connection of synovial IL-17 with IgA production in the joint. In this study we included synovial fluids (SF) from patients with rheumatoid arthritis (RA; n = 66), spondyloarthritis (SpA; n = 18) and osteoarthritis (OA; n = 36). The levels of IL-17, IL-6, transforming growth factor (TGF)-β1, B-cell-activating factor of the TNF family (BAFF) and anti-lipopolyssacharide (LPS) immunoglobulin (Ig)A were investigated by enzyme-linked immunosorbent assay (ELISA). Total IgA was measured by radial immunodiffusion assay. Synovial fluid-derived mononuclear cells (SFMC) were stimulated with bacterial antigens or SF-conditioned media, and cytokines and IgA were analyzed in the supernatants. IL-17, IL-6 and

Results: Salivary BAFF levels (median: 12.39 ng/ml) were significantly decreased by using HQ both at 12 (2.78 ng/ml, P = 0.008) and 24 weeks (0.54 ng/ml, P = 0.011). Similarly, decreases in serum BAFF levels (5.23 ng/ml) were seen at 12 and 24 weeks after HQ treatment (2.18 ng/ml, P = 0.008 and 0.0 ng/ml, P = 0.012, respectively). Serum and salivary BAFF levels were significantly lower in healthy controls (0.37 ng/ml and 0.0 ng/ml, resp.) compared to those of pSS before HQ therapy (P = 0.006 and P = 0.001, resp.). Unstimulated salivary flows were similar in patients treated with HQ after 12 (0.38 ml/min) and 24 weeks (0.50 ml/min) (P = 0.51) but higher than the patients rate at baseline (0.04 ml/min) (P = 0.008 ...

The maintenance of mature peripheral B cells depends on at least two survival cues, tonic signaling from the B cell receptor (BCR) complex and the extracellular cytokine B cell activating factor of the TNF family (BAFF). In addition to enhancing viability, BAFF controls the functional efficiency of the peripheral B cell pool by regulating complex physiological processes including cell growth, metabolism, energy homeostasis and entry into the cell cycle. BAFF-mediated induction of two molecular mechanisms, namely activation of the Akt signal transduction pathway and upregulation of the oncogenic kinase Pim-2 results in the modification of effector proteins including transcription factors and regulators of protein synthesis which are capable of executing the observed cellular physiological changes. The classic protein kinase C beta is instrumental in BAFF-induced Akt-activation and PKC beta-deficient B cells and mice show signs of partial refractiveness to BAFF. The protein tyrosine kinase Syk ...

Epstein-Barr virus ensures B cell survival by uniquely modulating apoptosis at early and late times after infection.s profile, publications, research topics, and co-authors

Belimumab is a human monoclonal antibody that selectively targets B-lymphocyte stimulator an important factor in the survival of B cells.

EGT1442 BAFF or Apr can induce activation sign in THP-1 cells which react to the excitement via production of the cytokine, IL-8, or a matrix degrading enzyme, MMP-9 (9,10). The siBAFF-transfected cells were EGT1442 tested for the responsiveness to BAFF or APRIL-mediated signaling then. As demonstrated in Fig. 2A, cells transfected with control siRNA taken care of immediately both anti-APRIL and anti-BAFF mAb and expressed large degrees of IL-8. Cells transfected with siBAFF didnt respond to the procedure with anti-BAFF mAb but taken care of immediately anti-APRIL mAb at a rate just like LPS response. The siBAFF-transfected cells had been after that treated with real estate agents that imitate its counterparts such as for example fusion protein including extracellular site of TACI (or BCMA) and Fc MYO5A part of human being immunoglobulin (TACI:Fc or BCMA:Fc). As demonstrated in Fig. 2A, both TACI:Fc and BCMA:Fc activated the cells expressing IL-8 at a rate slightly significantly less than that ...

Είναι το τελευταίο ποίημα του Σεφέρη και δημοσιεύτηκε στο Βήμα (23.9.71) τρεις μέρες μετά το θάνατό του στην περίοδο της δικτατορίας. Το ποίημα βασίζεται σε μια περικοπή του Πλάτωνα (Πολιτεία 614 κ.ε.) που αναφέρεται στη μεταθανάτια τιμωρία των αδίκων και ιδιαίτερα του Αρδιαίου. Ο Αρδιαίος, τύραννος σε μια πόλη, είχε σκοτώσει τον πατέρα του και τον μεγαλύτερο του αδερφό του. Γι αυτό και η τιμωρία του, καθώς και των άλλων τυράννων, στον άλλο κόσμο στάθηκε φοβερή. Όταν εξέτισαν την καθιερωμένη ποινή που επιβαλλόταν στους αδίκους και ετοιμαζόταν να βγουν στο ...

li data-cycle-auto-height=calc data-cycle-paused=false data-cycle-speed=500 data-cycle-next=#ticker-next data-cycle-prev=#ticker-prev data-cycle-fx=scrollVert data-cycle-log=false data-cycle-pause-on-hover=true data-cycle-timeout=2000 ...