1. TNFR signalling and its clinical implications
- Author
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Kay McNamee, Yi-Shu Huang, Hsi-Hsien Lin, Fiona E. McCann, Felix I.L. Clanchy, Shue-Fen Luo, Richard O. Williams, and Wen-Yi Tseng
- Subjects
0301 basic medicine ,Autoimmune disease ,business.industry ,medicine.medical_treatment ,Immunology ,Hematology ,medicine.disease ,Biochemistry ,Inflammatory bowel disease ,03 medical and health sciences ,Psoriatic arthritis ,030104 developmental biology ,0302 clinical medicine ,Immune system ,Cytokine ,Rheumatoid arthritis ,Psoriasis ,Immunology and Allergy ,Medicine ,Tumor necrosis factor alpha ,business ,Molecular Biology ,030217 neurology & neurosurgery - Abstract
Tumour necrosis factor-α (TNF-α) is a highly pleiotropic cytokine with effects on multiple pathological and physiological functions via two distinct receptors, TNFR1 and TNFR2. Much of the pro- inflammatory action of TNF-α is mediated by TNFR1 whereas TNFR2 is thought to play an immunoregulatory and tissue protective role. Anti-TNF- α biologics have been extremely successful in treating a number of immune mediated pathologies, including rheumatoid arthritis, ankylosing spondylitis, psoriasis, psoriatic arthritis and inflammatory bowel disease. However, anti-TNF therapy has been shown to induce systemic lupus erythematosus and psoriasis in some patients, and to be deleterious in multiple sclerosis. It is hypothesized that these paradoxical effects of anti-TNF-α are due to inhibition of TNFR2 signalling. In this review, we will focus on the biology and pathophysiologic role of TNF-α and on the therapeutic implications of targeting TNF-α receptor signalling.
- Published
- 2018