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Paradoxical effects of targeting TNF signalling in the treatment of autoimmunity

Nature Reviews Rheumatology volume 12, pages 625–626 (2016)Cite this article

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Adalimumab, an anti-TNF monoclonal antibody used to treat rheumatoid arthritis and other autoimmune disorders, paradoxically enhances the capacity of TNF to expand TNF receptor type II-expressing regulatory T cells. This provocative finding opens a new avenue for exploring the mechanisms that underlie efficacy, non-responsiveness and adverse effects associated with therapeutic targeting of TNF signalling.

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Figure 1: Expansion of regulatory T cells by targeting of TNF receptor type II.

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Acknowledgements

This research was supported (in part) by the Intramural Research Program of the US National Institutes of Health (NIH), National Cancer Institute, Center for Cancer Research. This project was also funded by University of Macau Research Grants (SRG2014-00024-ICMS-QRCM, and MYRG2016-00023-ICMS-QRCM) and a grant from the Science and Technology Development Fund (FDCT; Macao S.A.R. (014/2015/A1)).

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Authors and Affiliations

  1. State Key Laboratory of Quality Research in Chinese Medicine, Institute of Chinese Medical Sciences, University of Macau, Macao SAR 999078, China; and the Cancer and Inflammation Program, Center for Cancer Research, National Cancer Institute, Frederick, Maryland 21702, USA.,

    Xin Chen

  2. and the Cancer and Inflammation Program, Center for Cancer Research, National Cancer Institute, Frederick, Maryland 21702, USA.,

    Xin Chen

  3. Cancer and Inflammation Program, Center for Cancer Research, National Cancer Institute, Frederick, 21702, Maryland, USA

    Joost J. Oppenheim

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  1. Xin Chen
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Correspondence to Xin Chen or Joost J. Oppenheim.

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The authors declare no competing financial interests.

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Chen, X., Oppenheim, J. Paradoxical effects of targeting TNF signalling in the treatment of autoimmunity. Nat Rev Rheumatol 12, 625–626 (2016). https://doi.org/10.1038/nrrheum.2016.145

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