THURSDAY, Jan. 28 (HealthDay News) -- Infiltrating macrophages and interferons play a key role in the pathogenesis of glomerulonephritis, a complication of lupus characterized by abnormal growth of kidney cells leading to kidney damage, according to a study published online Jan. 26 in the Proceedings of the National Academy of Sciences.
To investigate the pathogenesis of glomerulonephritis in patients with systemic lupus erythematosus, Antigoni Triantafyllopoulou, M.D., of the Hospital for Special Surgery in New York City, and colleagues developed an accelerated mouse model of lupus nephritis.
The researchers found that the mice developed proliferative glomerulonephritis, characterized by infiltrating kidney macrophages that were responsible for the production of growth factors and renal matrix metalloproteinases, which were induced by type I interferon. Crescent formation was also dependent on kidney macrophages, according to the study. The macrophages were "alternatively activated macrophages," normally involved in tissue repair, rather than inflammatory macrophages.
"These findings reveal a role for type I interferons and alternatively activated macrophages in aggressive proliferative lesions of lupus nephritis," Triantafyllopoulou and colleagues conclude. "These findings suggest that manipulating kidney macrophage programming in lupus nephritis may represent a fruitful therapeutic approach to attenuating proliferative nephritis and associated irreversible renal cell loss and deterioration of function in systemic lupus erythematosus."
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