Primary B cells essentially lack constitutive NF-κB activity

Yedidia, Yifat; Ben‐Neriah, Yinon

doi:10.1002/(sici)1521-4141(199801)28:01<30::aid-immu30>3.3.co;2-8

Cited by 3 publications

(4 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…This would be in agreement with previous studies with 70Z/3 cells, where TGF‐β treatment of LPS‐stimulated cells blocked both κ gene and Oct‐2 expression but not NF‐κB activation, demonstrating that NF‐κB by itself is necessary but not sufficient to induce κ gene expression [24]. Our failure to detect NF‐κB in mature 70Z/3 cells is consistent with the finding that primary splenic mouse B cells lack constitutive NF‐κB binding activity [25], suggesting that the role of NF‐κB in B cells could be important for developmental cellular processes but not for the maintenance of the differentiated phenotype.…”

Section: Discussionsupporting

confidence: 93%

Possible stage‐specific function of NF‐κB during pre‐B cell differentiation

1998

View full text Add to dashboard Cite

Lipopolysaccharide (LPS)-induced differentiation of the murine pre-B cell line 70Z/3 is a model for pre-B to B cell differentiation and has been used to show that the transcription factor NF-U UB is essential to induce the expression of the IgU U gene. We have investigated the mechanism involved in late stages of the process when all cells have reached a more mature B phenotype, i.e. beyond 48 up to 96 h of LPS treatment. NF-U UB binding activity was induced at early times by LPS treatment, but its DNA binding activity disappeared after 84 h of LPS treatment. Accumulation of IU UBK K protein in the nucleus correlated with the disappearance of NF-U UB activity at 72, 84 and 96 h, and treatment of nuclear extracts of 72^96 h LPStreated cells with Na-deoxycholate restored NF-U UB binding activity. The data indicate that NF-U UB, while important to initiate the process of IgU U gene transcription in 70Z/3 pre-B cells, is no longer required for its maintenance in differentiated 70Z/3 cells.z 1998 Federation of European Biochemical Societies.

show abstract

Section: Discussionsupporting

confidence: 93%

Possible stage‐specific function of NF‐κB during pre‐B cell differentiation

1998

View full text Add to dashboard Cite

show abstract

“…CD80 is expressed in DCs, but not in resting B cells 29 . CD80 expression in B cells is induced by stimulation with LPS, CD154, cross‐linked CD21/CD35 or CD19 and partial inhibition of protein synthesis 12,30 , 31 .…”

Section: Discussionmentioning

confidence: 99%

“…Nuclear extraction was conducted as previously described 29 . Briefly, LPS‐stimulated B cells, irradiated or non‐irradiated, were washed and resuspended in 200–400 µl hypotonic buffer containing 10 m m Hepes (pH 7·9), 0·1 m m ethylenediaminetetraacetic acid (EDTA), 0·1 m m egtazic acid (EGTA), 10 m m KCl, 1 m m dithiothreitol (DTT), 0·75 m m spermidine, 0·15 m m spermine, 20 m m p ‐nitrophenyl phosphate, 20 m m β‐glycerophosphate, 1 m m Na 3 VO 4 , and protease inhibitors (1 m m phenylmethylsulphonyl fluoride, 5 µg/ml leupeptin, and 5 µg/ml peptstatin).…”

Section: Electrophoretic Mobility Shift Assay (Emsa)mentioning

confidence: 99%

See 1 more Smart Citation

Irradiation up‐regulates CD80 expression through two different mechanisms in spleen B cells, B lymphoma cells, and dendritic cells

Torihata

Ishikawa²,

Okada³

et al. 2004

Immunology

View full text Add to dashboard Cite

SUMMARYWe have previously demonstrated irradiation-induced up-regulation of CD80 expression in A20-HL B lymphoma cells by inducing expression of tumour necrosis factor-a (TNF-a) and CD154. In the present study, we investigated whether irradiation also up-regulates CD80 expression in mouse spleen B cells. Because freshly prepared spleen B cells are highly sensitive to irradiation, we employed spleen B cells stimulated with lipopolysaccharide (LPS-B cells). X-irradiation (8 Gy) followed by incubation (9-12 hr) highly and selectively up-regulated CD80 expression in LPS-B cells, whereas the same treatment slightly increased expression of CD54 and did not affect expression of CD86, major histocompatibility complex class II, CD11a or surface immunoglobulin M. The irradiation-induced up-regulation of CD80 expression resulted in enhanced APC function of LPS-B cells. Up-regulation of CD80 expression on LPS-B cells was accompanied by an increase in CD80 mRNA accumulation and nuclear factor (NF)-jB activation. Activation of NF-jB was shown to be critical for up-regulation of CD80 expression as pyrrolidine dithiocarbamate (PDTC), an inhibitor of NF-jB, severely decreased the observed up-regulation. X-irradiation of LPS-B cells induced expression of TNF-a but not CD154. However, anti-TNF-a monoclonal antibody (mAb) with anti-CD154 mAb did not inhibit X-irradiation-induced up-regulation of CD80 expression in LPS-B cells, whereas these mAbs almost completely inhibited this up-regulation in A20-HL cells and bone marrow-derived dendritic cells (DCs). In contrast, a thiol antioxidant, N-acetyl-L-cysteine, completely blocked X-irradiation-induced up-regulation of CD80 expression in LPS-B cells, but not in A20-HL cells or in DCs. Based on these findings, we concluded that X-irradiation up-regulates CD80 expression not only in A20-HL cells and DCs but also in LPS-B cells, and that this up-regulation in LPS-B cells via NF-jB activation is dependent on the generation of reactive oxygen species, while that in A20-HL cells and DCs is not.

show abstract

CpG Stimulation of Primary Mouse B Cells Is Blocked by Inhibitory Oligodeoxyribonucleotides at a Site Proximal to NF-κB Activation

Lenert¹,

Stunz²,

Yi³

et al. 2001

Antisense and Nucleic Acid Drug Development

103

View full text Add to dashboard Cite

Bacterial DNA and CpG-oligodeoxyribonucleotides (ODN) are powerful B cell activators, inducing apoptosis protection, cell cycle entry, proliferation, costimulatory molecule expression, immunoglobulin (Ig) and interleukin-6 (IL-6) secretion. However, proximal events in B cell activation by ODN are only partially characterized, including the translocation of NF-kappaB to the nucleus. In this paper, we provide evidence that CpG-ODN-induced cell cycle entry and apoptosis protection are blocked by SN50 or gliotoxin and thus require NF-kappaB activation. NF-kappaB activation occurred within 30 minutes of stimulation of murine B cells with a phosphorothioate (S) CpG-ODN and persisted for up to 40 hours, with p50, p65, and c-Rel as the major components. Similar to other NF-kappaB inducers, CpG-ODN caused an early IkappaBalpha and IkappaBbeta degradation plus cleavage of the p50 precursor and subsequent NF-kappaB nuclear translocation. A group of closely related S-ODN, which specifically blocked CpG-induced B cell activation at submicromolar concentrations, also prevented NF-kappaB DNA binding and transcriptional activation. These inhibitory S-ODN differed from stimulatory S-ODN by having 2-3 G substitutions in the central motif. As inhibitory S-ODN did not directly interfere with the NF-kappaB DNA binding but prevented CpG-induced NF-kappaB nuclear translocation of p50, p65, and c-Rel and blocked p105, IkappaBalpha, and IkappaBbeta degradation, we concluded that their putative target must lie upstream of inhibitory kinase (IKK) activation.

show abstract

Primary B cells essentially lack constitutive NF-κB activity

Cited by 3 publications

References 0 publications

Possible stage‐specific function of NF‐κB during pre‐B cell differentiation

Possible stage‐specific function of NF‐κB during pre‐B cell differentiation

Irradiation up‐regulates CD80 expression through two different mechanisms in spleen B cells, B lymphoma cells, and dendritic cells

CpG Stimulation of Primary Mouse B Cells Is Blocked by Inhibitory Oligodeoxyribonucleotides at a Site Proximal to NF-κB Activation

Contact Info

Product

Resources

About