Control of B Lymphocyte Apoptosis by the Transcription Factor NF-κB

Abstract

B cells maintain homeostasis by balancing cell viability and cell death. B lymphocytes are susceptible to mitochondria- and receptor-initiated cell death at various stages of peripheral differentiation and during immune responses. The inducible transcription factor NF-kappaB enhances cell viability by activating genes that counteract both cell-death pathways. This review uses characteristic features of NF-kappaB activation and downregulation to provide insight into the regulation of B cell apoptosis in the periphery. In particular, the temporal patterns of NF-kappaB induction, differences between Rel family members, and the intersection between canonical and noncanonical signaling pathways in keeping B cells alive are discussed.

miRNA profiling of B-cell subsets: specific miRNA profile for germinal center B cells with variation between centroblasts and centrocytes

“…40 By targeting IL-1 receptor-associated kinase and TNF receptor-associated factor 6, miR-146a causes a negative feedback for the Toll-like receptor signaling pathway. 40 As the role of NF-kB in B-cell homeostasis has been implicated in both immature B cell and also in maintaining GC function, 41 the strong miR-146a staining pattern that we observed in GC correlates with the functional role of NF-kB in the GC. However, the exact function of miR-146a in this pathway and how it might affect B cell survival should be further investigated.…”

Challenging Oneself Intermittently to Improve Health

“…The stress response pathways include those resulting in the activation of the transcription factors nuclear regulatory factor 2 (Nrf2), hypoxia inducible factor 1α (HIF-1α) and nuclear factor κB (NF-κB) and peroxisome proliferator activated receptors (PPARs) (Mattson and Meffert, 2006;Copple et al, 2010;Majmundar et al, 2010;Yessoufou and Wahli, 2010). Activation of the latter pathways results in increased production of a range of proteins including: antioxidant enzymes such as NAD(P)H quinone oxidoreductase (NQO1), superoxide dismutase 2, heme oxygenase 1 (HO-1) and glutathione peroxidase; erythropoietin and adiponectin; and the cell survival proteins Bcl-2 and Bcl-xL (Sen, 2006;Joshi and Johnson, 2012;Ong and Hausenloy, 2012). In addition, activation of PPARs can suppress inflammation by inhibiting the production of proinflammatory cytokines and cell adhesion molecules (Gervois and Mansouri, 2012).…”

NIK overexpression amplifies, whereas ablation of its TRAF3-binding domain replaces BAFF:BAFF-R-mediated survival signals in B cells

“…In mature resting B cells, both pathways of NF-B activation are induced and their generation and survival depends on both, demonstrated by gene disruption in the mouse at the level of transcription factors and signaling proteins (6,7).…”