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#28485798   2017/05/09 Save this To Up

Immune complexes induce TNF-α and BAFF production from U937 cells by HMGB1 and RAGE.

This study investigated the effects of immune complexes (ICs) on tumor necrosis factor α (TNF-α) and B cell-activating factor (BAFF) production from U937 cells and further explored the mechanism.

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#28331294   2017/03/23 Save this To Up

Spotlight on blisibimod and its potential in the treatment of systemic lupus erythematosus: evidence to date.

B cells in general and BAFF (B cell activating factor of the tumor necrosis factor [TNF] family) in particular have been primary targets of recent clinical trials in systemic lupus erythematosus (SLE). In 2011, belimumab, a monoclonal antibody against BAFF, became the first biologic agent approved for the treatment of SLE. Follow-up studies have shown excellent long-term safety and tolerability of belimumab. In this review, we critically analyze blisibimod, a novel BAFF-neutralizing agent. In contrast to belimumab that only blocks soluble BAFF trimer but not soluble 60-mer or membrane BAFF, blisibimod blocks with high affinity all three forms of BAFF. Furthermore, blisibimod has a unique structure built on four high-affinity BAFF-binding peptides fused to the IgG1-Fc carrier. It was tested in phase I and II trials in SLE where it showed safety and tolerability. While it failed to reach the primary endpoint in a recent phase II trial, post hoc analysis demonstrated its efficacy in SLE patients with higher disease activity. Based on these results, blisibimod is currently undergoing phase III trials targeting this responder subpopulation of SLE patients. The advantage of blisibimod, compared to its competitors, lies in its higher avidity for BAFF, but a possible drawback may come from its immunogenic potential and the anticipated loss of efficacy over time.

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#27994173   2016/12/20 Save this To Up

Transgenic overexpression of BAFF regulates the expression of immune-related genes in zebrafish, Danio rerio.

The B-cell activating factor (BAFF) is a member of tumour necrosis factor (TNF) superfamily that specifically regulates B lymphocyte proliferation and survival. Excess BAFF leads to overproduction of antibodies for secretion, anti-dsDNA antibodies and a lupus-like syndrome in mice. To investigate whether transgenic overexpression of the zebrafish BAFF leads to immunoglobulin changes and/or early maturing of the immune system, a Tol2-GFP-2A-BAFF/His recombinant plasmid was constructed by inserting a 2A peptide between the green fluorescent protein (GFP) and BAFF sequences. Functional GFP and BAFF proteins were expressed separately and confirmed in HeLa cells. The relative expression of immune-related genes (IgLC-1, IgLC-2, IgLC-3, IgD, IgM and IL-4), early lymphoid markers (Ikaros, Rag-1 and TCRAC), and the protooncogene Bcl-2 were evaluated by quantitative polymerase chain reaction (PCR) in F0 founder of transgenic zebrafish juveniles and adults. Ectopic expression of BAFF in adults was confirmed using Western blots and was shown to upregulate IgLC-1, IgLC-2, IgD, IgM, IgZ/T, Ikaros, Rag-1, TCRAC, IL-4 and Bcl-2 expression in juveniles on day 21 and IgLC-1, IgLC-2, IgD, IgM,IgZ/T, Rag-1, TCRAC and Bcl-2 expression in zebrafish three months postfertilization. The relative titers of specific IgM against Edwardsiella tarda WED were assessed using modified enzyme-linked immunosorbent assay (ELISA) with the whole body homogenate of zebrafish and demonstrated a significant increase in BAFF-transgenic group. Therefore, our findings provided novel insight into further exploration of modulating adaptive immunity and studying autoimmune diseases caused by regulating BAFF.

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#27774938   2016/10/24 Save this To Up

[miR-338-5p modulates B cell biological functions by targeting NF-κB1].

Objective To explore the effects of miR-338-5p on the nuclear factor κB1 (NF-κB1) expression and the IgG-producing ability of B cells. Methods Dual-luciferase reporter assay was used to test the target gene of miR-338-5p. The purified CD20(+) B cells were transfected with miR-338-5p agomiR, miR-338-5p antagomiR, NF-κB1 siRNA (siNF-κB1) and their corresponding negative control reagents, and then cultured with anti-IgM antibody and/or recombinant human B cell activating factor (rhBAFF). Real-time RCR and Western boltting were applied to determine the mRNA and protein levels of NF-κB1. IgG level in the supernatant was detected by ELISA. Results Compared with the control group, the hRluc/hLuc relative luciferase activity was significantly elevated in miR-338-5p mimic and NF-κB1-3'-UTR reporter co-transfected group. In the co-culture system with anti-IgM antibody and rhBAFF, the NF-κB1 mRNA, p105, p50 and IgG levels in B cells transfected with miR-338-5p agomiR were significantly increased, while the NF-κB1 mRNA and IgG levels in B cells transfected with miR-338-5p antagomiR were significantly decreased. The effect of siNF-κB1 on B cells was opposite to that of miR-338-5p agomiR. Correlation analysis suggested that NF-κB1 mRNA level was significantly positively correlated with IgG concentration. Conclusion miR-338-5p regulates the biological functions of B cells by positively regulating NF-κB1 expression and indirectly regulating BAFF signal.

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#27655102   2016/09/22 Save this To Up

B Cell-Activating Factor (BAFF)-Targeted B Cell Therapies in Inflammatory Bowel Diseases.

Inflammatory bowel diseases (IBD) involve dysregulated immune responses to gut antigens in genetically predisposed individuals. While a better elucidation of IBD pathophysiology has considerably increased the number of treatment options, the need for more effective therapeutic strategies remains a pressing priority. Defects of both non-hematopoietic (epithelial and stromal) and hematopoietic (lymphoid and myeloid) cells have been described in patients with IBD. Within the lymphoid system, alterations of the T cell compartment are viewed as essential in the pathogenesis of IBD. However, growing evidence points to the additional perturbations of the B cell compartment. Indeed, the intestinal lamina propria from IBD patients shows an increased presence of antibody-secreting plasma cells, which correlates with enhanced pro-inflammatory immunoglobulin G production and changes in the quality of non-inflammatory IgA responses. These B cell abnormalities are compounded by the emergence of systemic antibody responses to various autologous and microbial antigens, which predates the clinical diagnosis of IBD and identifies patients with complicated disease. It is presently unclear whether such antibody responses play a pathogenetic role, as B cell depletion with the CD20-targeting monoclonal antibody rituximab did not ameliorate ulcerative colitis in a clinical trial. However, it must be noted that unresponsiveness to rituximab is also observed also in some patients with autoimmune disorders usually responsive to B cell-depleting therapies. In this review, we discussed mechanistic aspects of B cell-based therapies and their potential role in IBD with a special interest on BAFF and BAFF-targeting therapies buoyed by the success of anti-BAFF treatments in rheumatologic disorders.

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#27568001   2016/08/28 Save this To Up

B cell activating factor is induced by toll-like receptor and NOD-like receptor-ligands and plays critical role in IgM synthesis in Labeo rohita.

B-cell activating factor (BAFF), an important member of the tumor necrosis factor superfamily, plays critical roles in the modulation of B-cell functions and enhancement of immune response in the host. Like higher vertebrates, the important role of BAFF in boosting immune response against diverse pathogens was also envisaged in fishes. We therefore, studied BAFF in rohu (Labeo rohita), a freshwater food fish species of highest economic importance in the Indian subcontinent. Full-length rohu-BAFF- cDNA comprised of 804bp nucleotide long ORF, encoding 267 amino acid residues, and shared high structural similarity with human-BAFF. It was expressed in the embryonic developmental stages suggesting its key role in immune response at the early life of fish. In Aeromonas hydrophila infection and rhabdoviral antigen stimulation, BAFF-gene expression in rohu was induced across the organs/tissues. Stimulation of un-treated healthy rohu fish leukocytes, and viral or bacterial or BSA (bovine serum albumin) antigen stimulated rohu fish leukocytes with recombinant-BAFF (r-BAFF) resulted in enhanced expression of immunoglobulin (Ig)M. Both in-vitro and in-vivo treatment with toll-like receptor (TLR)- ligand (poly I:C) or nod-like receptor (NLR)- ligands (iE-DAP and MDP) resulted in TLR and NLR activation and BAFF-gene expression. This is the first report showing BAFF-expression by innate immune receptor-ligands and its critical role in enhancing adaptive immune response in fish.

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#27500457   2016/09/05 Save this To Up

Bendamustine increases interleukin-10 secretion from B cells via p38 MAP kinase activation.

We investigated the effects of bendamustine on B cell functions and explored potential clinical applications of the drugs to autoimmune diseases. Proliferation of Ramos cells, a human B cell line, was significantly inhibited by 25-100μM of bendamustine in a dose-dependent manner. Concordantly, IgM secretion from Ramos cells was significantly inhibited at these concentrations by up to 70%. Interestingly, however, the production and secretion of interleukin-10 (IL-10) were dramatically (at least >10-fold) increased by bendamustine at growth inhibitory concentrations. Exploration of the molecular mechanism of IL-10 production revealed that bendamustine enhanced the phosphorylation of p38 MAP kinase. Further, Sp1 was identified as a downstream transcription factor, and the inhibition of p38 MAP kinase and Sp1 with their inhibitors led to the abrogation of bendamustine-induced IL-10 production and the DNA binding of Sp1. Importantly, when PBMC from healthy donors were cultured with bendamustine at the concentration of 30μM, under the stimulation with an anti-IgM antibody, an anti-CD40 antibody, recombinant human IL-21 (rhIL-21) and recombinant human soluble BAFF (rhsBAFF), IL-10 production by B cells (CD20+CD4-CD8-CD14-) among peripheral blood mononuclear cell (PBMC) was significantly enhanced by adding bendamustine. These results collectively suggest that the p38 MAP kinase-Sp1 pathway plays a crucial role in bendamustine-induced IL-10 production by B cells. Our findings suggest a novel therapeutic possibility for autoimmune diseases through the upregulation of IL-10 which has an anti-inflammatory effects.

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#27051973   2016/04/07 Save this To Up

Blisibimod for treatment of systemic lupus erythematosus: with trials you become wiser.

Blisibimod is a potent and selective inhibitor of B cell activating factor (BAFF), a mediator of differentiation, maturation and survival of B cells. It has a unique tetravalent, 'peptibody' structure and resulting high potency, and is currently in clinical evaluation for the treatment of SLE. The importance of BAFF in the pathogenesis of systemic lupus erythematosus (SLE) is under intense investigation. The anti BAFF monoclonal antibody belimumab was approved by the FDA for the treatment of SLE.

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#26914861   2016/02/27 Save this To Up

Binding of B-cell maturation antigen to B-cell activating factor induces survival of multiple myeloma cells by activating Akt and JNK signaling pathways.

B-cell maturation antigen (BCMA) is expressed on normal and malignant plasma cells and represents a potential target for therapeutic intervention. In this study, we characterized the mechanism underlying the protein kinase B (Akt) and c-Jun N-terminal kinase (JNK) pathways and BCMA interactions in regulating multiple myeloma (MM) cell survival. It was found that the expression levels of B cell-activating factor (BAFF) and BCMA were increased in MM cells as compared with those in normal controls. The proliferation of U266 cells was induced by recombinant human BAFF (rhBAFF) and could also be decreased by BCMA siRNA. The expression of Bcl-2 protein was up-regulated, and Bax protein was down-regulated after rhBAFF treatment, which could be reversed by BCMA siRNA. Similarly, the protein p-JNK and p-Akt were activated by rhBAFF and could be changed by BCMA siRNA. In addition, the BCMA mRNA and protein expression levels were decreased after treatment with Akt and JNK pathway inhibitors. These results suggest that Akt and JNK pathways are involved in the regulation of BCMA. A novel BAFF/BCMA signalling pathway in MM may be a new therapeutic target for MM.

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#26749059   2016/03/10 Save this To Up

Participation of B-cell-activating factor receptors in the pathogenesis of immune thrombocytopenia.

ESSENTIALS: Dysfunctional B-cell-activating factor (BAFF) system is related to many autoimmune diseases. The regulatory functions of BAFF/BAFF receptors were investigated in an in vitro coculture system. Different regulatory roles of BAFF were investigated via different receptors in immune thrombocytopenia. The upregulated BAFF receptors on autoreactive lymphocytes lead to their hypersensitivity to BAFF.

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