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MALT1 directs B cell receptor-induced canonical nuclear factor-kappaB signaling selectively to the c-Rel subunit

Uta Ferch1, Christian Meyer zum Büschenfelde, Andreas Gewies

  • 1Third Medical Department, Technical University of Munich, Klinikum rechts der Isar, 81675 Munich, Germany.

Nature Immunology
|July 31, 2007
PubMed

Insights

Bcl-10 and MALT1 scaffold proteins differentially regulate immune cell signaling. Bcl-10 is crucial for B cell receptor-induced activation, apoptosis blocking, and proliferation, while MALT1 selectively controls c-Rel signaling.

Area of Science:

  • Immunology
  • Molecular Biology
  • Cell Signaling

Background:

  • Nuclear factor-kappaB (NF-kappaB) transcription factors are key regulators of immune cell responses.
  • Scaffold proteins Bcl-10 and MALT1 link antigen receptor signaling to the canonical NF-kappaB pathway, playing critical roles in lymphomagenesis.

Purpose of the Study:

  • To investigate the differential roles of Bcl-10 and MALT1 in B cell receptor-induced NF-kappaB signaling.
  • To elucidate the specific mechanisms by which Bcl-10 and MALT1 control the activation of RelA and c-Rel transcription factors.

Main Methods:

  • Analysis of B cell receptor-induced signaling pathways.
  • Investigating the recruitment of the IKK kinase complex into lipid rafts.
  • Assessing the impact of Bcl-10 and MALT1 on RelA and c-Rel activation, apoptosis, and cell proliferation.

Main Results:

  • Bcl-10 is essential for IKK recruitment to lipid rafts, leading to RelA and c-Rel activation, apoptosis inhibition, and cell division following B cell receptor ligation.
  • MALT1 contributes to survival signaling but is not involved in IKK recruitment or activation, and is dispensable for RelA induction and proliferation.
  • MALT1 selectively activates c-Rel, controlling a distinct signaling subprogram.

Conclusions:

  • Bcl-10 and MALT1 exhibit distinct functions in regulating B cell receptor-induced survival and proliferation signals.
  • The study provides mechanistic insights into the selective control of c-Rel within the canonical NF-kappaB pathway by MALT1.

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