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

Academic Article


  • 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 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 β integrin-deficient (CD18-null) MRL/ MpJ-Fas mice, suggesting a lack of redundancy among the β 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. lpr lpr 2 2
  • Authors

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    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