NF-kappa B1 p50 is required for BLyS attenuation of apoptosis but dispensable for processing of NF-kappa B2 p100 to p52 in quiescent mature B cells

J Immunol. 2003 Jul 15;171(2):761-8. doi: 10.4049/jimmunol.171.2.761.

Abstract

B lymphocyte stimulator (BLyS), a TNF family protein essential for peripheral B cell development, functions primarily through attenuation of B cell apoptosis. In this study, we show that BLyS activates NF-kappaB through both classical and alternative pathways with distinct kinetics in quiescent mature B cells. It rapidly and transiently enhances the p50/p65 DNA binding activity and induces phosphorylation of IkappaBalpha characteristic of the classical NF-kappaB pathway, albeit maintaining IkappaBalpha at a constant level through ongoing protein synthesis and proteasome-mediated destruction. With delayed kinetics, BLyS promotes the processing of p100 to p52 and sustained formation of p52/RelB complexes via the alternative NF-kappaB pathway. p50 is dispensable for p100 processing. However, it is required to mediate the initial BLyS survival signals and concomitant activation of Bcl-x(L) in quiescent mature B cells ex vivo. Although also a target of BLyS activation, at least one of the A1 genes, A1-a, is dispensable for the BLyS survival function. These results suggest that BLyS mediates its survival signals in metabolically restricted quiescent B cells, at least in part, through coordinated activation of both NF-kappaB pathways and selective downstream antiapoptotic genes.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Animals
  • Apoptosis / genetics
  • Apoptosis / immunology*
  • B-Cell Activating Factor
  • B-Lymphocyte Subsets / cytology
  • B-Lymphocyte Subsets / metabolism*
  • Cell Differentiation / genetics
  • Cell Differentiation / immunology
  • Cell Survival / genetics
  • Cell Survival / immunology
  • I-kappa B Proteins / metabolism
  • Interphase / genetics
  • Interphase / immunology*
  • Membrane Proteins / physiology*
  • Mice
  • Mice, Inbred C57BL
  • Mice, Knockout
  • Minor Histocompatibility Antigens
  • NF-KappaB Inhibitor alpha
  • NF-kappa B / antagonists & inhibitors
  • NF-kappa B / deficiency
  • NF-kappa B / genetics
  • NF-kappa B / metabolism*
  • NF-kappa B / physiology*
  • NF-kappa B p50 Subunit
  • NF-kappa B p52 Subunit
  • Phosphorylation
  • Protein Biosynthesis
  • Protein Processing, Post-Translational / genetics
  • Protein Processing, Post-Translational / immunology*
  • Proto-Oncogene Proteins c-bcl-2 / deficiency
  • Proto-Oncogene Proteins c-bcl-2 / genetics
  • Proto-Oncogene Proteins c-bcl-2 / metabolism
  • Signal Transduction / genetics
  • Signal Transduction / immunology
  • Transcription Factor RelA
  • Tumor Necrosis Factor-alpha / physiology*
  • Up-Regulation / genetics
  • Up-Regulation / immunology
  • bcl-X Protein

Substances

  • B-Cell Activating Factor
  • BCL2-related protein A1
  • Bcl2l1 protein, mouse
  • I-kappa B Proteins
  • Membrane Proteins
  • Minor Histocompatibility Antigens
  • NF-kappa B
  • NF-kappa B p50 Subunit
  • NF-kappa B p52 Subunit
  • Nfkbia protein, mouse
  • Proto-Oncogene Proteins c-bcl-2
  • Tnfsf13b protein, mouse
  • Transcription Factor RelA
  • Tumor Necrosis Factor-alpha
  • bcl-X Protein
  • NF-KappaB Inhibitor alpha