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| Content Provider | Springer Nature Link |
|---|---|
| Author | Kodama, S. Davis, M. Faustman, D. L. |
| Copyright Year | 2005 |
| Abstract | Excess levels of tumor necrosis factor-α (TNF-α) have been associated with certain autoimmune diseases. Under the rationale that elevated TNF-α levels are deleterious, several anti-TNF-α therapies are now available to block the action of TNF-α in patients with autoimmune diseases with a chronic inflammatory component to the destructive process. TNF-α antagonists have provided clinical benefit to many patients, but their use also is accompanied by new or aggravated forms of autoimmunity. Here we propose a mechanistically based hypothesis for the adverse events observed with TNF-α antagonists, and argue for the opposite therapeutic strategy: to boost or restore TNF-α activity as a treatment for some forms of autoimmunity. Activation defects in the transcription factor nuclear factor κB leave autoreactive T cells sensitive to TNF-α-induced apoptosis. Treatment with TNF-α, by destroying autoreactive T cells, appears to be a highly targeted strategy to interrupt the pathogenesis of type 1 diabetes, lupus and certain forms of autoimmunity. |
| Starting Page | 1850 |
| Ending Page | 1862 |
| Page Count | 13 |
| File Format | |
| ISSN | 1420682X |
| Journal | Cellular and Molecular Life Sciences |
| Volume Number | 62 |
| Issue Number | 16 |
| e-ISSN | 14209071 |
| Language | English |
| Publisher | Birkhäuser-Verlag |
| Publisher Date | 2005-06-17 |
| Publisher Place | Basel |
| Access Restriction | Subscribed |
| Subject Keyword | NF-κB TNF-α apoptosis autoimmunity Life Sciences Biomedicine general Biochemistry Cell Biology |
| Content Type | Text |
| Resource Type | Article |
| Subject | Cell Biology Molecular Biology Molecular Medicine Pharmacology Cellular and Molecular Neuroscience |
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