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Reduced late endosome/lysosome function promotes SLE through chronic PI3K activity and SHP-1/SHIP-1 defects.

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Summary

Systemic lupus erythematosus (SLE) patients show impaired late endosome and lysosome (LEL) acidification, leading to cellular waste buildup and immune complex accumulation. This dysfunction may serve as a biomarker for specific SLE disease types.

Keywords:
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Area of Science:

  • Immunology
  • Cell Biology
  • Pathophysiology

Background:

  • Cellular waste degradation relies on hydrolases activated by late endosome and lysosome (LEL) acidification.
  • Dysfunctional LEL acidification is implicated in various diseases.

Purpose of the Study:

  • To investigate LEL acidification and its association with disease activity and biomarkers in Systemic Lupus Erythematosus (SLE).

Main Methods:

  • Cross-sectional study of SLE patients and a murine model (MRL/lpr mice).
  • Analysis of LEL acidification, surface-bound nucleosome and IgG-immune complex (IgG-IC) accumulation.
  • Investigated mechanistic pathways involving PI3k, SHP-1, and SHIP-1.

Main Results:

  • SLE patients exhibit diminished LEL acidification and increased surface nucleosome accumulation on immune cells.
  • Active SLE correlates with impaired LEL acidification and IgG-IC exocytosis.
  • Murine models and specific molecular deficiencies (SHP-1, SHIP-1) recapitulate LEL dysfunction.
  • Non-acidic LELs are found in 67% of SLE patients and associate with specific clinical manifestations (arthritis, rash, nephritis).

Conclusions:

  • LEL dysfunction is a frequent finding in SLE, associated with active disease and specific clinical features.
  • LEL dysfunction may represent a distinct endotype in SLE.
  • LEL dysfunction has the potential to serve as a valuable biomarker for SLE patient stratification.