## Abstract The pro‐inflammatory cytokines tumor necrosis factor (TNF) and interleukin‐1 (IL‐1) have been shown to be primary mediators in the pathogenesis of chronic inflammatory joint diseases. However, the relative contributions of these molecules to the development and progression of disease is
Tumor necrosis factor (TNF) receptor type 2 mediates thymocyte proliferation independently of TNF receptor type 1
✍ Scribed by Matthias Grell; Florian M. Becke; Harald Wajant; Daniela N. Männel; Peter Scheurich
- Publisher
- John Wiley and Sons
- Year
- 1998
- Tongue
- English
- Weight
- 112 KB
- Volume
- 28
- Category
- Article
- ISSN
- 0014-2980
No coin nor oath required. For personal study only.
✦ Synopsis
Tumor necrosis factor (TNF) mediates its biological effects by binding to two distinct but homologous receptor molecules. The type 1 receptor (TNF-R1) has been shown to be essential and sufficient for most cellular responses to soluble TNF. In contrast, only limited data exist concerning the role of the type 2 receptor (TNF-R2) in TNF responses, both in vitro and in vivo. Here, we demonstrate by the use of thymocytes from TNF-R-deficient mice that the TNF-R2-dependent enhancement of proliferation and secretion of granulocyte-macrophage colony-stimulating factor is in fact mediated by TNF-R2 on its own, independent of co-expression and/or stimulation of TNF-R1.
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