A team of researchers, at the University of Texas Southwestern Medical Center, Dallas, and Uppsala University, Sweden, has shed new light on several forms of the kidney disease known as nephritis.
Specifically, the data indicate a protective role for kallikrein proteins in anti-GBM antibody–induced nephritis (a mouse model of Goodpasture syndrome) and spontaneous lupus nephritis in mice and humans.
In the study, which was led by Chandra Mohan, Edward Wakeland, and Marta Alarcón-Riquelme, kallikrein genes were found to be underexpressed in the kidneys of mouse strains sensitive to anti-GBM antibody–induced nephritis.
Conversely, mouse strains that upregulated kallikreins in the kidneys showed fewer signs of disease. Consistent with this, antagonizing the kallikrein pathway enhanced disease and agonists dampened disease severity.
As both human systemic lupus erythematosus and spontaneous lupus nephritis were found to be associated with kallikrein genes, the authors conclude that kallikreins are protective disease-associated genes in anti-GBM antibody–induced nephritis and lupus.
In an accompanying commentary, Claudio Ponticelli and Pier Luigi Meroni, at IRCCS Istituto Clinico Humanitas, Italy, discuss this possibility and suggest alternative roles for kallikreins in lupus nephritis.
The research is published in the March 23, 2009, issue of the Journal of Clinical Investigation.
Materials provided by Journal of Clinical Investigation. Note: Content may be edited for style and length.
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