Disease-associated amyloid and misfolded protein aggregates activate the inflammasome

作者:Masters Seth L*; O'Neill Luke A J
来源:Trends in Molecular Medicine, 2011, 17(5): 276-282.
DOI:10.1016/j.molmed.2011.01.005

摘要

The pathogenesis of type 2 diabetes, Alzheimer's disease and amyotrophic lateral sclerosis continues to be debated. Recently, the inflammasome protein complex has been shown to be a key regulator of IL-1 beta, a cytokine implicated in each of these diseases. In all three cases, it is now apparent that unique protein aggregates caused by inappropriate oligomerization or misfolding are sensed by the inflammasome, providing a unifying mechanism for this IL-1 beta production. What evolved as an innate defense against infection-related particles, therefore, now seems to be a driving force for inflammation in these diseases. This review discusses the basic research behind these findings and the potential for new therapeutic interventions this affords.

  • 出版日期2011-5