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. 2022 Feb 4;44(4):445–459. doi: 10.1007/s00281-022-00910-2

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© The Author(s) 2022

Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 2 — Overview of the different functions of TNFR1 and TNFR2. TNFR1 is activated by sTNF and mTNF whereas TNFR2 is preferentially activated by mTNF. TNFR1 contains a death domain and can therefore execute cell death signals. TNFR1 signalling that leads to the activation of NFκB (cf. Fig. 1) mediates inflammation as well as cell survival and proliferation. TNFR2 does not contain a death domain. Recruitment of TRAF1 and 2 as well as cIAP1 and 2 to the intracellular domain of TNFR2 results in canonical and, via activation of NFκB-inducing kinase (NIK), to non-canonical NFκB activation. Besides induction of inflammation, cell survival, and proliferation, TNFR2 was supposed to cooperate with TNFR1 to induce cell death by down-modulation of TRAF2 and cIAPs, thereby inhibiting the anti-apoptotic NFκB signalling pathway (not shown, see text). Moreover, it has been assumed that mTNF might function as receptor for an activating antibody, thereby inducing apoptosis by reverse signalling (see text)