CARD-BCL-10-MALT1 signalling in protective and pathological immunity

Jürgen Ruland1, Lara Hartjes2

  • 1Institute of Clinical Chemistry and Pathobiochemistry, School of Medicine, Technical University of Munich, Munich, Germany. j.ruland@tum.de.

Nature Reviews. Immunology
|November 24, 2018
PubMed

Insights

CARD protein-BCL-10-MALT1 (CBM) signalosomes regulate immune responses by forming filaments that control inflammatory gene expression. Dysregulation of CBM signaling is linked to immune diseases and cancers.

Area of Science:

  • Immunology
  • Molecular Biology
  • Cell Signaling

Background:

  • CARD protein-BCL-10-MALT1 (CBM) signalosomes are crucial multiprotein platforms controlling immune and inflammatory pathways.
  • These complexes are essential for host defense and maintaining tissue homeostasis.
  • Genetic alterations in CBM signaling components are implicated in various immune-mediated diseases.

Purpose of the Study:

  • To review the regulation and signaling mechanisms of CBM complexes.
  • To discuss the physiological roles of CBM signaling in host defense and homeostasis.
  • To explore the pathophysiological functions of CBM complexes in immune-related diseases and cancers.

Main Methods:

  • Literature review of CBM signalosome function.
  • Analysis of CBM complex assembly and protease activity.
  • Examination of CBM signaling in immune and inflammatory contexts.

Main Results:

  • CBM signalosomes form self-organizing filaments upon immune activation.
  • CBM complexes regulate canonical nuclear factor-κB (NF-κB) and mitogen-activated protein kinase (MAPK) pathways.
  • Two layers of inflammatory gene expression control are mediated by CBM signaling, including mRNA-binding protein degradation.

Conclusions:

  • CBM signalosomes play a vital role in immune regulation and tissue homeostasis.
  • Understanding CBM signaling is critical for addressing immune deficiencies, inflammatory disorders, and lymphoid malignancies.
  • Further research into CBM complexes may reveal therapeutic targets for immune-mediated diseases.

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