Lupus & antiphospholipid syndrome

Elevated integrin αvβ3 expression activates the NF-κB p65/p100 pathway and promotes inflammatory responses in systemic lupus erythematosus

Clin Exp RheumatolPublished Mechanistic study

Authors' conclusion

This study highlights that the upregulation of integrin αvβ3 expression in SLE activates the NF-κB p65/p100 pathway, which plays a pivotal role in orchestrating inflammatory responses.

Study context

Population
Patients with systemic lupus erythematosus (SLE), healthy controls and MRL/lpr lupus mice
Participants
36 vs 36
Comparison
Patients with SLE vs healthy controls; integrin αvβ3 antagonist SB273005 in MRL/lpr lupus mice
  • SLEn = 36
  • Healthy controln = 36reference
Methodological detailsin vivo and in vitro, MRL/lpr lupus mouse model, Western blot and immunohistochemistry staining, Student's t-test, ANOVA and post-hoc Kruskal-Wallis tests
  • In vivo and in vitro
  • MRL/lpr lupus mouse model
  • Western blot and immunohistochemistry staining
  • Student's t-test, ANOVA and post-hoc Kruskal-Wallis tests

Main finding

As reported in the abstract

  • Elevated integrin αvβ3 expression in serum, skin and renal tissues of patients with SLE, contributing to NF-κB activation
  • Enhanced synthesis of NF-κB p65 and p100, promoting NF-κB activation and dysregulation of TLR7 expression
  • Increase in inflammatory factors such as TNF-α and IL-6, making skin and kidneys more susceptible to inflammation
  • SB273005 in MRL/lpr mice significantly reduced NF-κB p65/p100 synthesis, suppressed NF-κB activation, decreased inflammatory factors in serum and kidneys and alleviated organ damage

Original publication

Elevated integrin αvβ3 expression activates the NF-κB p65/p100 pathway and promotes inflammatory responses in systemic lupus erythematosus. Clin Exp Rheumatol. Published 26 January 2025. doi:10.55563/clinexprheumatol/0cfcsp

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