FRIDAY, Feb. 15 (HealthDay News) --Pathways regulating apoptosis, or programmed cell death, are altered in patients with systemic lupus erythematosus (SLE), and mice with particular mutations in these pathways develop a lupus-like disease, according to a study published online Feb. 14 in Immunity.
Jack Hutcheson of Saint Louis University in St. Louis and colleagues examined the balance between the Bcl-2 and Fas apoptotic pathways in patients with systemic lupus erythematosus and in mouse models of the disease.
The researchers found that mononuclear cells from lupus patients had increased expression of anti-apoptotic members of the Bcl-2 and Fas pathways. Mice that lacked a pro-apoptotic Bcl-2 family member and had a particular mutation in Fas developed a severe lupus-like disease at 16 weeks, in contrast to mice bearing either alone. Even though large numbers of markedly activated antigen-presenting cells (APCs) were found in lymphoid tissues and kidneys of these mice, there were many apoptotic cells in the glomeruli.
"These data demonstrate that dysregulation of the Bcl-2 or Fas pathways can alter the function of APCs, thereby leading to SLE pathogenesis," Hutcheson and colleagues conclude.