T helper-17 (TH17) cells express the transcription factor RORγt, produce IL-17 and IL-22, and are required for defense against extracellular pathogens and to sustain the integrity of epithelial barrier surfaces [1]. However, unrestrained TH17 cell responses have been implicated in autoimmune disease pathogenesis [2, 3]. A network of transcription factors control TH17 differentiation, including RORγt [4] and members of the NF-κB family [5]. The canonical NF-κB pathway is necessary to initiate T cell activation [6], while noncanonical NF-κB is critical for balancing TH lineage decisions [7]. Activation of the non-canonical NF-κB pathway depends on the stabilization of NF-κB inducing Kinase (NIK), which is regulated by the E3 ubiquitin ligases cIAP1 and cIAP2 [8].
cIAP1/2 antagonization by SMAC mimetic induces non‐canonical NF‐κB mediated TH17 cell homotypic interactions and increases their resistance to shear stress
John Rizk,Rasmus Agerholm,Alexander Jönsson,A. Doğan,M. Dufva,Vasileios Bekiaris
Published 2021 in European Journal of Immunology
ABSTRACT
PUBLICATION RECORD
- Publication year
2021
- Venue
European Journal of Immunology
- Publication date
2021-05-07
- Fields of study
Biology, Medicine
- Identifiers
- External record
- Source metadata
Semantic Scholar, PubMed
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