## Abstract ## Background Rheumatoid arthritis (RA) is a chronic autoimmune disease that causes inflammation and destruction of the joints. In the collagenβinduced arthritis mouse model of RA, we developed a nonviral gene therapy method designed to block __in situ__ the main cytokine tumour necros
Effect of tumour necrosis factor in the mouse-tail model of psoriasis
β Scribed by K. Nagano; K. Hori; T. Nagane; T. Sugawara; J. Oh-ishi; H. Hayashi; N. Watanabe; Y. Niitsu
- Publisher
- Springer-Verlag
- Year
- 1990
- Tongue
- English
- Weight
- 891 KB
- Volume
- 282
- Category
- Article
- ISSN
- 0340-3696
No coin nor oath required. For personal study only.
β¦ Synopsis
The effects of local and systemic administration of tumour necrosis factor (TNF) on the mouse-tail model of psoriasis were examined histologically at 4 days after administration. Subcutaneous injection of TNF at 1 x 101 to 1 β’ 10 4 units/mouse resulted in dose-dependent formation of a granular layer in the tail scales, which was quantified as the percentage of tail scales having granular layer formations extending over half or more of their surface and was larger than that occurring in untreated mice and in mice receiving injections of vehicle solution alone. Daily intraperitoneal injection of TNF at 1 x 103 or 1 x 10 4 units/mouse for 28 days resulted in similar granular layer formation and in a significantly reduced mitotic index of the tail keratinocytes, indicating an antiproliferative effect of TNF. The lowered mitotic index and the induction of granular layers, apparently attributable to a modulation of keratinocyte proliferation and differentiation by TNF, suggest that TNF may be effective as a drug for treatment of psoriasis.
π SIMILAR VOLUMES
Tumonr necrosis factor alpha (TNF~) effectively stimulates the oxidative metabolism of human PMN in vitro. Moreover, preincnbation of PMN with TNF~ has been shown to result in an altered response of the target cells to subsequent stimulation. In the present study the response of PMN to stimulation i