cIAP1/2 antagonization by SMAC mimetic induces non-canonical NF-κB mediated TH 17 cell homotypic interactions and increases their resistance to shear stress

John Rizk; Rasmus Agerholm; Alexander Jönsson; Asli Aybike Dogan; Martin Dufva; Vasileios Bekiaris

doi:10.1002/eji.202048983

cIAP1/2 antagonization by SMAC mimetic induces non-canonical NF-κB mediated T_H 17 cell homotypic interactions and increases their resistance to shear stress

Eur J Immunol. 2021 Aug;51(8):2097-2099. doi: 10.1002/eji.202048983. Epub 2021 May 27.

Authors

John Rizk¹, Rasmus Agerholm¹, Alexander Jönsson¹, Asli Aybike Dogan¹, Martin Dufva¹, Vasileios Bekiaris¹

Affiliation

¹ Department of Health Technology, Technical University of Denmark, Lyngby, Denmark.

PMID: 33960415
DOI: 10.1002/eji.202048983

Abstract

SMAC antagonization of cIAP1/2 in T_H 17 cells upregulates cell adhesion and cytoskeleton genes through the NIK-RelB and p52 axis. SMAC also increases the homotypic interactions of T_H 17 cells through a non-canonical NF-κB- and integrin-mediated mechanism resulting in increased ability of T_H 17 cells to withstand shear stress.

Keywords: NF-κB; SMAC; TH17; cIAP1/2; shear stress.

Publication types

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

MeSH terms

Apoptosis Regulatory Proteins / metabolism*
Baculoviral IAP Repeat-Containing 3 Protein / antagonists & inhibitors
Cell Adhesion / physiology
Humans
Inhibitor of Apoptosis Proteins / antagonists & inhibitors
Lymphocyte Activation / physiology
Mitochondrial Proteins / metabolism*
NF-kappa B / metabolism*
Signal Transduction / immunology*
Th17 Cells / metabolism*

Substances

Apoptosis Regulatory Proteins
DIABLO protein, human
Inhibitor of Apoptosis Proteins
Mitochondrial Proteins
NF-kappa B
Baculoviral IAP Repeat-Containing 3 Protein