Special Issue "Tumor Necrosis Factor (TNF)"
A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".
Deadline for manuscript submissions: closed (28 February 2019)
Tumor Necrosis Factor (TNF) and its receptors TNFR1 and TNFR2 are the best characterized members of the TNFSF and TNFRSF superfamilies, which include, to date, 19 ligands and 29 receptors. TNFSF members share the common ability to promote pro-inflammatory signals, but they might regulate other cellular functions, such as cell-to-cell communication, differentiation, survival, apoptosis and necroptosis. TNF activates several intracellular signaling pathways, mainly NF-kB, JNK, apoptosis (caspase 8 activation) and necroptosis (phosphorylation of RIPK1, RIPK3 and of MLKL), of which constant balance regulates the opposite cell fates, proliferation or death.
TNF, mainly produced by macrophages, NK and Th1 T lymphocytes, has a central role in innate and adaptive immunity and in chronic inflammatory diseases, such as those of the joints, mainly rheumatoid arthritis and spondiloarthris, and those of the intestine, namely the inflammatory bowel diseases. Chronic inflammation including the TNF-TNFR pathway activation, is increasingly recognized as involved also in cancer, obesity, diabetes, cardiovascular diseases and neurodegenerative disorders. Five drugs blocking the TNF-TNFR signaling have been approved for the therapy of chronic inflammatory rheumatic and intestinal diseases, but the number of these drugs and the number of diseases, which might benefit from this type of treatment, is expected to largely increase in the near future. This Special Issue on “Tumor Necrosis Factor (TNF)” addresses the biology of TNF-TNFR pathway, the newest knowledge on its role in diseases characterized by chronic inflammation and on established and emerging therapies targeting TNF signaling.
Prof. Dr. Daniela Basso
Manuscript Submission Information
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- Tumor Necrosis Factor
- Tumor Necrosis Factor Receptors
- Metabolic syndrome
- Anti-TNF agents