NDLI: Complement factor H and the hemolytic uremic syndrome

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Complement factor H and the hemolytic uremic syndrome

Content Provider	Scilit
Author	Atkinson, John P. Goodship, Timothy H. J.
Copyright Year	2007
Description	Immune recognition is coupled to powerful proinflammatory effector pathways that must be tightly regulated. The ancient alternative pathway of complement activation is one such proinflammatory pathway. Genetic susceptibility factors have been identified in both regulators and activating components of the alternative pathway that are associated with thrombotic microangiopathies, glomerulonephritides, and chronic conditions featuring debris deposition. These observations indicate that excessive alternative pathway activation promotes thrombosis in the microvasculature and tissue damage during debris accumulation. Intriguingly, distinct genetic changes in factor H (FH), a key regulator of the alternative pathway, are associated with hemolytic uremic syndrome (HUS), membranoproliferative glomerulonephritis (dense deposit disease), or age-related macular degeneration (AMD). A mouse model of HUS designed to mirror human mutations in FH has now been developed, providing new understanding of the molecular pathogenesis of complement-related endothelial disorders.
Related Links	https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2118604/pdf
Ending Page	1248
Page Count	4
Starting Page	1245
DOI	10.1084/jem.20070664
Journal	The Journal of experimental medicine
Issue Number	6
Volume Number	204
Language	English
Publisher	Rockefeller University Press
Publisher Date	2007-06-04
Access Restriction	Open
Subject Keyword	Urology and Nephrology Model Debris Complement Hemolytic Uremic Syndrome Hus Proinflammatory Journal: The Journal of experimental medicine (Vol- 204, Issue- 6)
Content Type	Text
Resource Type	Article

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