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This study assessed TNFRSF13C expression on leukaemic cells ofchildhood B-cell precursor acute lymphoblastic leukaemia patients. Of note, during the early drug treatment, its expression is maintained or even increased on residual tumour cells, suggesting a positive selection and survival of TNFRSF13C positive blast cells.
the B-cell receptor BR3 modulates cellular branching via Rac1 during neuronal migration
Expression patterns of BAFF and its receptor BAFF-R differ according to lupus nephritis class.
up-regulated expression in intractable temporal lobe epilepsy
Inhibition of ADAM10 augments BAFF-dependent survival of primary human B cells, whereas inhibition of ADAM17 increases BAFFR expression levels.
Relationships between serum BAFF and BBR expression [(BAFFR, calcium signal modulating cyclophilic ligand interactor (TACI) and B cell maturation antigen (BCMA)] were determined on B cell subsets, defined using immunoglobulin (Ig)D/CD38. Twenty pre-RTX and 18 rheumatoid arthritis patients relapsing after B cell depletion were included.
Among the BAFF receptors in a cohort of rheumatoid arthritis (RA) patients, the AA have shown, by fluorescence activated cell sorter (FACS) analysis of median fluorescence intensity (MFI), that transmembrane activator and calcium-modulating cyclophilin ligand interactor (TACI) and B cell maturation antigen (BCMA) do not change
The expression levels of serum BAFF and the three receptors (TACI, BCMA and BAFF-R) in non-Hodgkin lymphoma patients were significantly higher than in healthy controls.
Variants in BAFF-R gene is associated with chronic lymphocytic leukemia.
BAFF-R, as the principal receptor of BAFF, not only decreased the apoptosis of B cells and CD8+ T cells by upregulating the expression of Bcl-2 and BclxL, but also promoted B-cell proliferation in immune thrombocytopenia.
genetic polymorphism contributes to the pathogenesis of primary antibody deficiency
BAFF and BAFF-R are expressed in the thyrocytes derived from patients with either autoimmune thyroid disorders or multinodular goiter, as well in the infiltrating immune cells of Graves' disease and Hashimoto's thyroiditis
There is an increased prevalence of the BAFF-R His159Tyr mutation in patients with Sjogren's syndrome (SS), particularly in those with SS complicated by MALT lymphoma whose disease onset occurred at a younger age.
Expression of mutant caspase-9 correlated with a downregulation of BAFFR (B-cell-activating factor belonging to the TNF family (BAFF) receptor) in B cells and ICOS (inducible T-cell costimulator) in T cells.
Variants of TNFRSF13C were associated with common variable immunodeficiency.
Negative expression of BAFF-R, but not of BAFF, could be an independent risk factor for progression-free survival and Overall survival in patients with diffuse large B-cell lymphoma treated with standard R-CHOP.
the common TLR4-D299G, TLR4-T399I and BAFFR-P21R polymorphisms provide the carriers with a protective advantage against ICU-acquired sepsis; this finding was more profound for medical patients compared to trauma or surgical ones
Data show significant differences in expression of tumour necrosis factor family (BAFF) receptors BAFF-R, BCMA and TACI in patients with and without anti-Jo-1 or anti-Ro52/anti-Ro60 autoantibodies.
In view of the restricted expression of the BAFF-R on normal cells and the multiple anti-pre-B ALL activities stimulated by this antibody, a further examination of its use for treatment of pre-B ALL is warranted.
Availability of BAFF determines BAFF-R and TACI expression on B cells in common variable immunodeficiency.
results indicate that the BAFF-BAFFR ligation bridged between microglia and neurons could play a critical neuroprotective role in brain ischemic injuries
These findings elucidate a crucial molecular pathway of B cell selection in the earliest phases of activation by identifying a novel link between B cell receptor affinity and BAFF-R signaling towards Mcl-1.
B cell-activating factor (BAFF) upregulates CD28/B7 and CD40/CD154 expression, and promotes the interactions between T and B cells in a BAFF receptor-dependent manner.
conclude that P44S BAFFR mutation does not hinder BAFFR function or enhance B cell activity in MRL/Lpr and MRL mice and that other susceptibility loci on the MRL background contributed to the hyperactivity of these cells
Results from this study suggest blockade of CXCL13 and BAFFR together may be an effective therapeutic strategy in preventing salivary hypofunction and reducing autoantibody titers and sialadenitis in patients with Sjogren's syndrome
Heteromers consisting of one BAFF and two APRIL bind to receptor TACI, BCMA but not to BAFFR.
Syk-deficient B cells require BAFF receptor and CD19/PI3K signaling for their long-term survival.
In conclusion, BAFFR signaling affects both innate and adaptive immune activation during viral infections.
BAFF controls neural cell survival through BAFF receptor.
BAFF receptor deficiency limits Murid herpesvirus 4 infection.
Although we have found that TACI is dispensable for controlling B. hermsii infection, mice deficient in BAFFR or BAFF exhibit impairment in B. hermsii-specific IgM responses and clearance of bacteremia.
tnfrsf13c is dispensable for the development of SLE in NZM mice.
Data show that the B cell antigen receptor (BCR) and Igalpha may be required for B cell survival because they function as adaptor proteins in a BAFFR signaling pathway leading to activation of Syk, indicating crosstalk between the two receptors.
BAFF downregulates the expression of steatogenesis genes and enhances steatosis in hepatocytes through BAFF-R.
BAFF-R deficiency in mice selectively alters mature B2 cell-dependent cellular and humoral immune responses and limits the development of atherosclerosis.
Targeting the BAFF-R to specifically reduce atherogenic B2 cell numbers while preserving atheroprotective B1a cell numbers may be a potential therapeutic strategy to reduce atherosclerosis by potently reducing arterial inflammation.
Soluble BAFF levels inversely correlate with peripheral B cell numbers and the expression of BAFF receptors.
These findings indicate that upregulation of TLR7 may augment BAFF secretion by APC and through ligation of BAFF-R promote autoreactive B cell survival and thus anti-platelet autoantibody production.
BLyS receptor expression and downstream signaling were normal in CD22(-/-) B cells, suggesting that CD22 does not directly alter BLyS responsiveness
our data indicate that BAFFR and tonic BCR signals cooperate to enable nonautoreactive immature B cells to differentiate into transitional B cells and to be positively selected into the naive B cell repertoire.
B cell-activating factor (BAFF) enhances B-cell survival in vitro and is a regulator of the peripheral B-cell population. Overexpression of Baff in mice results in mature B-cell hyperplasia and symptoms of systemic lupus erythematosus (SLE). Also, some SLE patients have increased levels of BAFF in serum. Therefore, it has been proposed that abnormally high levels of BAFF may contribute to the pathogenesis of autoimmune diseases by enhancing the survival of autoreactive B cells. The protein encoded by this gene is a receptor for BAFF and is a type III transmembrane protein containing a single extracellular cysteine-rich domain. It is thought that this receptor is the principal receptor required for BAFF-mediated mature B-cell survival.
tumor necrosis factor receptor superfamily, member 13C
, tumor necrosis factor receptor superfamily member 13C
, B cell-activating factor receptor
, B-cell-activating factor receptor
, BAFF receptor
, BLyS receptor 3
, B-cell maturation defect 1
, b cell-activating factor receptor