title: Crosstalk between TNF and glucocorticoid receptor signaling pathways.
abstract: TNF is a Janus-faced protein. It possesses impressive anti-tumor activities, but it is also one of the strongest known pro-inflammatory cytokines, which hampers its use as a systemic anti-cancer agent. TNF has been shown to play a detrimental role in inflammatory diseases such as rheumatoid arthritis and inflammatory bowel disease. Glucocorticoids are strongly anti-inflammatory and exert their therapeutic effects through binding to their receptor, the glucocorticoid receptor. Therefore, glucocorticoids have been used for over half a century for the treatment of inflammatory diseases. However, many patients are or become resistant to the therapeutic effects of glucocorticoids. Inflammatory cytokines have been suggested to play an important role in this steroid insensitivity or glucocorticoid resistance. This review aims to highlight the mechanisms of mutual inhibition between TNF and GR signaling pathways.
authors.affiliation: Department of Biomedical Molecular Biology, Ghent University, Belgium.
authors.forename: Tom
authors.initials: T
authors.lastname: Van Bogaert
authors.forename: Karolien
authors.initials: K
authors.lastname: De Bosscher
authors.forename: Claude
authors.initials: C
authors.lastname: Libert
mesh_terms: D000893:Anti-Inflammatory Agents / Q000378:metabolism / Q000494:pharmacology / Q000627:therapeutic use; D006801:Humans; D007249:Inflammation / Q000188:drug therapy; D020239:Receptor Cross-Talk; D011965:Receptors, Glucocorticoid / Q000187:drug effects / Q000378:metabolism / Q000502:physiology; D015398:Signal Transduction / Q000187:drug effects*; D014409:Tumor Necrosis Factor-alpha / Q000037:antagonists & inhibitors*
chemical_list: D000893:Anti-Inflammatory Agents; D011965:Receptors, Glucocorticoid; D014409:Tumor Necrosis Factor-alpha