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Soluble CD95L triggers calcium responses and Th17 cell accumulation in lupus. Ritonavir and novel peptidomimetics disrupt this interaction, alleviating lupus symptoms in mice.

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Area of Science:

  • Immunology
  • Molecular Biology
  • Pharmacology

Background:

  • Soluble CD95L (s-CD95L) binding to CD95 induces calcium responses via PLCγ1, promoting Th17 cell accumulation and lupus pathology.
  • This pathway differs from membrane-bound CD95L (m-CD95L)-induced apoptosis, highlighting a distinct role in autoimmune disease.

Purpose of the Study:

  • To investigate the role of the CD95-PLCγ1 interaction in lupus pathogenesis.
  • To identify therapeutic agents that disrupt this interaction and ameliorate lupus symptoms.

Main Methods:

  • Large-scale screening to identify inhibitors of the CD95-PLCγ1 interaction.
  • Structure-activity relationship analysis of identified inhibitors.
  • Synthesis of CD95-derived peptidomimetics.
  • In vivo studies using lupus mouse models.

Main Results:

  • Ritonavir, an HIV protease inhibitor, was identified as a potent disruptor of the CD95-PLCγ1 interaction.
  • Ritonavir acts as a peptidomimetic, mimicking the calcium-inducing domain (CID) of CD95 for PLCγ1 docking.
  • Synthesized CID peptidomimetics effectively abrogated CD95-mediated calcium responses and Th17 cell transmigration.
  • Treatment with ritonavir or CID peptidomimetics alleviated clinical symptoms in lupus mice.

Conclusions:

  • The CD95-PLCγ1 signaling pathway is a key driver of lupus pathology.
  • Ritonavir and novel CID peptidomimetics represent a promising new therapeutic strategy for lupus.
  • Targeting this pathway offers a novel avenue for drug development in autoimmune diseases.