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HSP90β controls NLRP3 autoactivation.

Lotte Spel1, Cyrielle Hou1, Katerina Theodoropoulou1,2

  • 1Department of Immunobiology, University of Lausanne, 155 Ch. des Boveresses, Epalinges 1066, Switzerland.

Science Advances
|February 28, 2024
PubMed
Summary
This summary is machine-generated.

The HSP90β-SGT1 complex is essential for NLRP3 inflammasome activation in cryopyrin-associated periodic syndromes (CAPS). Inhibiting HSP90β may treat CAPS by reducing IL-1β secretion.

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Area of Science:

  • Immunology
  • Molecular Biology
  • Genetics

Background:

  • Gain-of-function mutations in NLRP3 cause cryopyrin-associated periodic syndromes (CAPS).
  • NLRP3 inflammasome activation leads to inflammatory cytokine release, but its precise mechanisms remain unclear.
  • Understanding NLRP3 regulation is key to developing targeted therapies for autoinflammatory diseases.

Purpose of the Study:

  • To identify key regulators of NLRP3 inflammasome assembly using a functional genetic approach.
  • To investigate the role of the HSP90β-SGT1 chaperone complex in NLRP3 inflammasome activation.
  • To explore therapeutic strategies targeting HSP90β for CAPS treatment.

Main Methods:

  • Functional genetic screening to identify regulators of NLRP3 inflammasome formation.
  • Assessing the impact of HSP90β and HSP90α deficiency on ASC speck formation.
  • Evaluating the effect of nigericin and alum stimulation on inflammasome assembly.
  • Testing HSP90β inhibitors on peripheral blood mononuclear cells (PBMCs) from CAPS patients.

Main Results:

  • The HSP90β-SGT1 chaperone complex was identified as crucial for NLRP3 inflammasome activation in CAPS.
  • HSP90β deficiency impaired ASC speck formation, while HSP90α deficiency had no significant effect.
  • Stimulation with nigericin or alum bypassed the requirement for SGT1 and HSP90β, indicating alternative pathways.
  • Pharmacological inhibition of HSP90β reduced pathological IL-1β secretion in CAPS patient PBMCs.

Conclusions:

  • The HSP90β-SGT1 complex plays a critical role in a specific pathway of NLRP3 inflammasome activation relevant to CAPS.
  • Targeting HSP90β offers a potential therapeutic strategy for CAPS, aiming to reduce excessive inflammation.
  • This approach may preserve physiological NLRP3 functions while mitigating disease-specific hyperactivation.