IL-17 receptor goes solo in autoimmune inflammation

Stefan Bittner; Frauke Zipp

doi:10.1016/j.immuni.2023.08.007

IL-17 receptor goes solo in autoimmune inflammation

Immunity. 2023 Sep 12;56(9):1977-1980. doi: 10.1016/j.immuni.2023.08.007.

Authors

Stefan Bittner¹, Frauke Zipp²

Affiliations

¹ Department of Neurology, Focus Program Translational Neuroscience (FTN) and Immunotherapy (FZI), Rhine-Main Neuroscience Network (rmn(2)), University Medical Center of the Johannes Gutenberg University Mainz, Mainz, Germany.
² Department of Neurology, Focus Program Translational Neuroscience (FTN) and Immunotherapy (FZI), Rhine-Main Neuroscience Network (rmn(2)), University Medical Center of the Johannes Gutenberg University Mainz, Mainz, Germany. Electronic address: zipp@uni-mainz.de.

PMID: 37703825
DOI: 10.1016/j.immuni.2023.08.007

Abstract

IL-17-blocking antibodies have shown little clinical effect in some autoimmune diseases such as multiple sclerosis. In this issue of Immunity, Luo et al. demonstrate that SHP2-Act1 complexes can mediate autonomous IL-17R signaling in the absence of the IL-17 ligand itself.

Publication types

Research Support, Non-U.S. Gov't
Comment

MeSH terms

Antibodies, Blocking
Autoimmune Diseases*
Humans
Inflammation
Interleukin-17*
Receptors, Interleukin-17

Substances

Interleukin-17
Receptors, Interleukin-17
Antibodies, Blocking