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Comment
. 2014 Jan 7;111(1):E3-4.
doi: 10.1073/pnas.1321248111. Epub 2013 Dec 31.

Role for terminal complement activation in amyotrophic lateral sclerosis disease progression

Trent M Woodruff  1 , John D Lee, Peter G Noakes
Affiliations
Comment

Role for terminal complement activation in amyotrophic lateral sclerosis disease progression

Trent M Woodruff et al. Proc Natl Acad Sci U S A. .
No abstract available

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Fig. 1.
Fig. 1.
The C5a receptor CD88 contributes to disease progression in the SOD1G93A genetic model of ALS. Kaplan–Meier plot of ages (in days) in which SOD1G93A mice with normal (CD88+/+, orange line) or fully deleted (CD88−/−, blue line) CD88 reached end-stage of disease (complete hindlimb paralysis and an inability to right itself once placed on its back) in males (A) and females (B). Average (±SEM) ages of the disease end stages are also shown. SOD1G93A mice lacking C5a signaling via CD88 show a significant extension in survival compared with control SOD1G93A mice in both sexes, demonstrating a pathogenic role for C5a in this mutant ALS mouse model. n = 24 mice per group: P = 0.0002 (A) and P = 0.002 (B), log-rank test.
See this image and copyright information in PMC

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References

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