Loss of LFA-1, but not Mac-1, protects MRL/MpJ-Faslpr mice from autoimmune disease

Academic Article

Abstract

  • Systemic lupus erythematosus (SLE) is an autoimmune disease characterized by immune complex-mediated tissue injury. Many different adhesion molecules are thought to participate in the development of SLE; however, few studies have directly examined the contributions of these proteins. Here we demonstrate that LFA-1 plays an essential role in the development of lupus in MRL/MpJ-fas lpr mice. Mice deficient in LFA-1, but not Mac-1, showed significantly increased survival, decreased anti-DNA autoantibody formation, and reduced glomerulonephritis. The phenotype of the LFA-1-deficient mice was similar to that observed in β2 integrin-deficient (CD18-null) MRL/ MpJ-Faslpr mice, suggesting a lack of redundancy among the β2 integrin family members and other adhesion molecules. These studies identify LFA-1 as a key contributor in the pathogenesis of autoimmune disease in this model, and further suggest that therapeutic strategies targeting this adhesion molecule may be beneficial for the treatment of SLE.
  • Published In

    Digital Object Identifier (doi)

    Author List

  • Kevil CG; Hicks MJ; He X; Zhang J; Ballantyne CM; Raman C; Schoeb TR; Bullard DC
  • Start Page

  • 609
  • End Page

  • 616
  • Volume

  • 165
  • Issue

  • 2