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

Guerrini, Luisa; Molteni, Angela; Blasi, Francesco

doi:10.1016/s0014-5793(98)00965-x

Cited by 6 publications

(4 citation statements)

References 33 publications

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“…NF-B-specific complexes were also identified by EMSA (data not shown). These results are consistent with those obtained with virally transformed preB cells (Sen and Baltimore, 1986;Guerrini et al, 1998) or IL-7-stimulated late preB cells (Kistler et al, 1998). Therefore, the first criterion supporting a role for Fig.…”

Section: Discussionsupporting

confidence: 92%

The Role of NF-κB as a Survival Factor in Environmental Chemical-Induced Pre-B Cell Apoptosis

et al. 2001

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Polycyclic aromatic hydrocarbons (PAH) are ubiquitous environmental chemicals that suppress the immune system at multiple levels, including at the level of B cell development in the bone marrow microenvironment. Specifically, PAH induce preB cell apoptosis in primary bone marrow cultures and in cocultures of an early preB cell line (BU-11) and a bone marrow stromal cell line (BMS2). Previous studies focused on the molecular mechanisms through which PAH induce stromal cells to deliver an apoptosis signal to adjacent preB cells. Apoptosis signaling within the preB cell itself was not investigated. Here, the role of NF-kappaB, a lymphocyte survival factor, in PAH-induced preB cell apoptosis was assessed. Analysis of DNA-binding proteins extracted from the nuclei of untreated BU-11 cells indicated DNA-binding complexes comprising NF-kappaB subunits p50, c-Rel, and/or Rel A. NF-kappaB down-regulation with previously described inhibitors induced BU-11 cell apoptosis, demonstrating that the default apoptosis pathway blocked by NF-kappaB is functional at this early stage in B cell development. Similarly, exposure of BU-11/BMS2 cocultures to 7,12-dimethylbenz[a]anthracene (DMBA), a prototypic PAH, down-regulated nuclear Rel A and c-Rel before overt apoptosis. Finally, ectopic expression of Rel A or c-Rel rescued BU-11 cells from DMBA-induced apoptosis. These results extend previous observations by demonstrating that 1) NF-kappaB is a survival factor at an earlier stage of B cell development than previously appreciated and 2) NF-kappaB down-regulation is likely to be part of the molecular mechanism resulting in PAH-induced preB cell apoptosis. These results suggest nonclonally restricted, PAH-mediated suppression of B lymphopoiesis.

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Section: Discussionsupporting

confidence: 92%

The Role of NF-κB as a Survival Factor in Environmental Chemical-Induced Pre-B Cell Apoptosis

et al. 2001

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“…These observations agree with results obtained from earlier studies indicating that the transcription factor families NF‐κB/Rel are of importance in the regulation of cytokine production. 26‐31 T cells from c‐Rel knock‐out mice fail to respond to activation and proliferation signals mediated by the TCR and mitogens. 32 The mechanism behind the decreased LPS activation of NF‐κB in cells incubated with catecholamines is not yet clear.…”

Section: Discussionmentioning

confidence: 99%

Nuclear Factor‐κB is Involved in the Catecholaminergic Suppression of Immunocompetent Cells

Bergquist

Ohlsson

Tarkowski

2000

Annals of the New York Academy of Sciences

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A BSTRACT : Catecholamines are known to exert a powerful impact on the immune system by downregulation of proliferation and differentiation, and induction of apoptosis. However, the mechanism for this regulatory route is still unclear. Therefore well established human monocytic cell-lines and nontransformed human monocytes, obtained from peripheral blood, were incubated with an optimal concentration of LPS and varying concentrations of the catecholamine dopamine. The proliferative response to LPS was determined by [ 3 H]thymidine incorporation, and a significant suppressive effect by dopamine was obtained. LPS-induced binding of NF-B to DNA, determined by electrophoretic mobility shift assay, was inhibited by extrinsic dopamine, leading to a decreased proliferation and cytokine expression. In contrast, the intracellular ceramide concentration was not affected by incubation of peripheral blood lymphocytes with dopamine. Our findings suggest that the NF-B-I-B transcription machinery may well be involved in the catecholaminergic regulation of the immune system, while the ceramide-SAPK/JNK cascade appears not to play a significant role in this suppression.

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“…EMSA was done as previously described [24]. Equivalent amounts of nuclear protein (5 Ag) were incubated on ice for 10 min in a buffer containing 12.5 mM HEPES, pH 7.9, 0.5 mM EDTA, 50 mM KCl, 1 mM MgCl 2 , 10% Ficoll, and 2.5 Ag poly-dIdC (Amersham, Uppsala, Sweden).…”

Section: Electrophoretic Mobility-shift Assay (Emsa)mentioning

confidence: 99%

Dysregulated interleukin-8 secretion and NF-κB activity in human cystic fibrosis nasal epithelial cells

Carrabino

Carpani

Livraghi

et al. 2006

Journal of Cystic Fibrosis

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

Cited by 6 publications

References 33 publications

The Role of NF-κB as a Survival Factor in Environmental Chemical-Induced Pre-B Cell Apoptosis

The Role of NF-κB as a Survival Factor in Environmental Chemical-Induced Pre-B Cell Apoptosis

Nuclear Factor‐κB is Involved in the Catecholaminergic Suppression of Immunocompetent Cells

Dysregulated interleukin-8 secretion and NF-κB activity in human cystic fibrosis nasal epithelial cells

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