Table 1.
Tumour necrosis factor alpha (TNFα) blockade in experimental glomerulonephritis (GN) and vasculitis
| Author | Model | Agent | Outcome |
|---|---|---|---|
| Karkar [17] | SD rat NTN | sTNFr p55 | Reduced glomerular inflammation and IL-1β expression |
| Lan [18] | SD rat NTN | TNF binding protein | Reduced glomerular inflammation and MIF expression |
| Karkar [19] | WKY rat NTN | sTNFr p55 | Prevention: abrogation of crescents Treatment: reduced crescents and IL-1β |
| Khan [20] | WKY rat NTN | Anti-TNFα mAb | Prevention: reduced crescents and urine MCP-1 Treatment: reduced glomerular injury and interstitial scarring |
| Le Hir [21] | TNF−/− mouse NTN | – | Knockout protected from crescents |
| Timoshanko [22] | TNF−/− chimeric mice NTN | – | Intrinsic renal cells major source of TNF with contribution from leucocytes |
| Little [23] | WKY rat EAV | Anti-TNFα mAb | Abrogation of crescents Improvement lung haemorrhage Inhibition leucocyte transmigration |
| Huugen [24] | Mouse anti-MPO GN | Anti-TNFα mAb | Reduced glomerular inflammation |
SD, Sprague-Dawley; WKY, Wistar Kyoto; NTN, nephrotoxic nephritis; EAV, experimental autoimmune vasculitis; MPO, myeloperoxidase; MIF, migration inhibitory factor; sTNFr, soluble TNF receptor; MCP-1, monocyte chemoattractant protein 1.