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Exposure of cultured human glomerular mesangial cells (GMC) to normal human serum and an activator of the complement system results in rapid uptake of the terminal complement proteins C5b-9 by the cells. This 'innocent bystander' complement attack, however, does not result in cell killing, but in the stimulation of the GMC to release prostaglandin E (PGE), interleukin 1 (Il-1) and tumor necrosis factor (TNF). Endogenously synthesized Il-1 in turn activates PGE release, indicating that the C5b-9 attack initiates an autocrine feedback stimulation. Together with the fact that C5b-9 is found in many forms of glomerulonephritis, the data point to a role of the terminal complement proteins in the initiation and perpetuation of an inflammatory response.
M Schönermark, and
R Deppisch, and
G Riedasch, and
K Rother, and
G M Hänsch
September 1991,
The American journal of physiology,
M Schönermark, and
R Deppisch, and
G Riedasch, and
K Rother, and
G M Hänsch
January 1994,
Experimental nephrology,
M Schönermark, and
R Deppisch, and
G Riedasch, and
K Rother, and
G M Hänsch
April 1990,
Kidney international,
M Schönermark, and
R Deppisch, and
G Riedasch, and
K Rother, and
G M Hänsch
October 1997,
Journal of immunology (Baltimore, Md. : 1950),
M Schönermark, and
R Deppisch, and
G Riedasch, and
K Rother, and
G M Hänsch
November 1989,
The American journal of physiology,
M Schönermark, and
R Deppisch, and
G Riedasch, and
K Rother, and
G M Hänsch
July 1986,
Clinical and experimental immunology,
M Schönermark, and
R Deppisch, and
G Riedasch, and
K Rother, and
G M Hänsch
May 1993,
The Journal of clinical investigation,
M Schönermark, and
R Deppisch, and
G Riedasch, and
K Rother, and
G M Hänsch
March 2001,
Kidney international,
M Schönermark, and
R Deppisch, and
G Riedasch, and
K Rother, and
G M Hänsch
November 1995,
The American journal of physiology,
M Schönermark, and
R Deppisch, and
G Riedasch, and
K Rother, and
G M Hänsch
June 2006,
Life sciences,
