Cell Death-Related Ubiquitin Modifications in Inflammatory Syndromes: From Mice to Men

Nieves Peltzer; Alessandro Annibaldi

doi:10.3390/biomedicines10061436

Cell Death-Related Ubiquitin Modifications in Inflammatory Syndromes: From Mice to Men

Biomedicines. 2022 Jun 17;10(6):1436. doi: 10.3390/biomedicines10061436.

Authors

Nieves Peltzer^{1

2

3}, Alessandro Annibaldi¹

Affiliations

¹ Center for Molecular Medicine Cologne (CMMC), University of Cologne, Robert-Koch-Strasse 21, 50931 Köln, Germany.
² Department of Translational Genomics, University of Cologne, Weyertal 115b, 50931 Köln, Germany.
³ Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases (CECAD) Research Center, University of Cologne, Joseph-Steltzmann-Strasse 26, 50931 Köln, Germany.

Abstract

Aberrant cell death can cause inflammation and inflammation-related diseases. While the link between cell death and inflammation has been widely established in mouse models, evidence supporting a role for cell death in the onset of inflammatory and autoimmune diseases in patients is still missing. In this review, we discuss how the lessons learnt from mouse models can help shed new light on the initiating or contributing events leading to immune-mediated disorders. In addition, we discuss how multiomic approaches can provide new insight on the soluble factors released by dying cells that might contribute to the development of such diseases.

Keywords: A20; LUBAC; OTULIN; apoptosis; autoimmunity; cell death; human genetics; inflammation; necroptosis; pyroptosis; ubiquitin.

Publication types

Review

Grants and funding

This work was funded by the Deutsche Forschungsgemeinschaft (DFG, German Research Foundation, project no. AN 1717/1-1), the Jürgen Manchot Foundation, and the CMMC Junior Research Group Program for A.A.; N.P. is supported by Deutsche Forschungsgemeinschaft (DFG, German Research Foundation; project SFB1399, ID 413326622) and the Jürgen Manchot Foundation. Both N.P. and A.A. are supported by the collaborative research centres SFB1430, ID. 414786233 (A10 for N.P. and associated project for A.A.) and SFB1503, ID 455784452 (B02 for N.P. and A05 for A.A.).