Table 3.
Amyloid deposition in C1q knockout and factor B/C2 knockout mice
| Amyloid deposition | ||||
|---|---|---|---|---|
| Liver | Spleen | |||
| Genotype | 125I-SAP retained* | Amyloid score† | 125I-SAP retained* | Amyloid score† |
| Wild type n = 20 | 10·0 (6·0) | 1 (0–3) | 1·5 (0·4) | 3 (2–3) |
| Factor B/C2 knockout n = 19 | 9·4 (4·3) P = 0·8112 | 1 (0–2) P = 0·5838 | 1·5 (0·8) P = 0·7787 | 3 (0–3) P = 0·9552 |
| C1q knockout n = 23 | 7·4 (3·2) P = 0·9903 | 1 (1–3) P = 0·1886 | 1·5 (0·6) P = 0·9903 | 3 (2–3) P = 0·7516 |
All mice received AEF and AgNO3 on day 0 as described in Methods.
*
Mean (SD),% injected dose of125I-labelled human SAP retained in organs at death on day 3, after intravenous tracer injection on day 2.
†
Median (range), histological grade of congophilic amyloid deposits assessed as in Methods.
P-values are for Wilcoxon rank sum (Mann–Whitney) tests between each knockout group and the wild type controls. One way anova tests comparing radiolabelled SAP retention among all three groups gave P = 0·1567 for the livers and P = 1·000 for the spleens.