Clinical mouse models of lupus
Mouse model | Autoantibodies | Clinical manifestation | |||||||
Glomerulonephritis | Arthritis | Skin rash | Others | Advantages | Disadvantages | References | |||
Spontaneous models | NZB/NZW F1 (BW) |
| Active proliferative (4–5 months) | Absent | Absent | Vasculitis | Accelerated by IFN |
| 15 16 |
MRL/lpr |
| Active proliferative (3–4 months) | Microscopic synovitis | Rash on face and back | Cognitive dysfunction, vasculitis and oophoritis | Early and severe disease onset with several clinical manifestations observed in humans |
| 20 | |
MRL/+ |
| Nephritis (very late in life) | Mild microscopic synovitis | Mild dermatitis | Late cognitive dysfunction |
| 19 | ||
BXSB |
| Proliferative (4–5 months) | Absent but neutrophilic infiltrate in joints | Absent | Evaluation of TLR-7 driven mechanisms |
| 28 | ||
Induced models | Pristane |
| Active proliferative nephritis (6–8 months post induction) | Erosive arthritis | Rash on face | Hepatitis, pulmonary vasculitis, anaemia and serositis | Induced in non-autoimmune strain Predictable timing |
| 32–34 |
Resiquimod |
| Proliferative nephritis (at 4 weeks post induction) | Absent | Absent | Splenomegaly, carditis, hepatitis | No gender predominance Rapid onset |
| 36 | |
Imiquimod |
| Proliferative nephritis | Absent | Dermatitis | Atherosclerosis |
BW, black−white; dsDNA, anti-double stranded DNA; Fas, cell surface death receptor; IFN, interferon; lpr, lymphoproliferation; MRL, Murphy-Roths-Large; NZ, New Zealand; Sm, Smith; SnRNP, small nuclear ribonucleoprotein; TLR, toll-like receptor.