K < sub > 2P < /sub > 2.1 is a regulator of inflammatory cell responses in idiopathic inflammatory myopathies

In this study, we investigated the role of K2P2.1 in the autoimmune response of IIMs. We detected K2P2.1 expression in primary skeletal muscle and endothelial cells of murine and human origin. We observed an increased pro-inflammatory cell response, adhesion and transmigration by pharmacological blockade or genetic deletion of K2P2.1 in vitro and in in vivo myositis mouse models. Of note, our findings were not restricted to endothelial cells as skeletal muscle cells with impaired K2P2.1 function also demonstrated a strong pro-inflammatory response. Conversely, these features were abrogated by activation of K2P2.1 and improved the disease course of a myositis mouse model. In humans, K2P2.1 expression was diminished in IIM patients compared to non-diseased controls arguing for the translatability of our findings. In summary, K2P2.1 may regulate the inflammatory response of skeletal muscle. Further research is required to understand whether K2P2.1 could serve as novel therapeutic target.PMID:37935063 | DOI:10.1016/j.jaut.2023.103136

Source: Journal of Autoimmunity - November 7, 2023 Category: Allergy & Immunology Authors: Christopher Nelke Thomas M üntefering Derya Cengiz Lukas Theissen Vera Dobelmann Christina B Schroeter Helena Block Corinna Preu ße Alexander P E Michels Stefanie Lichtenberg Marc Pawlitzki Steffen Pfeuffer Niklas Huntemann Alexander Zarbock Thorben Bri Source Type: research