Survival signaling in resting B cells

Curr Opin Immunol. 2004 Apr;16(2):251-5. doi: 10.1016/j.coi.2004.01.007.

Abstract

The survival of mature resting B cells in the periphery depends on signaling from the B-cell receptor (BCR) and the B-cell activating factor of the TNF family receptor (BAFF-R). Engagement of both receptors promotes NF-kappa B activity, which contributes to B-cell survival through different pathways. BCR signaling leads to activation of the inhibitor of NF-kappa B kinase (IKK) complex via Carma1, Bcl10 and MALT1, whereas BAFF-R engagement promotes processing of NF-kappa B2 protein p100, which is dependent on NF-kappa B-inducing kinase (NIK) and IKK alpha. Proximal signaling intermediates are potentially common to both pathways. We suggest that BCR and BAFF-R survival signaling are mutually dependent. In addition, we propose that BAFF-R signaling enhances the expression of survival genes through direct chromatin modifications in NF-kappa B target gene promoters.

Publication types

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

MeSH terms

  • Animals
  • B-Cell Activation Factor Receptor
  • B-Lymphocytes / metabolism*
  • Cell Survival
  • Membrane Proteins / metabolism
  • Mice
  • NF-kappa B / metabolism
  • Receptors, Tumor Necrosis Factor / metabolism
  • Signal Transduction*

Substances

  • B-Cell Activation Factor Receptor
  • Membrane Proteins
  • NF-kappa B
  • Receptors, Tumor Necrosis Factor
  • Tnfrsf13c protein, mouse