Card9/neutrophil signalling axis promotes IL-17A-mediated ankylosing spondylitis.

ABSTRACT:

Objective

Polymorphisms in the antifungal signalling molecule CARD9 are associated with ankylosing spondylitis (AS). Here, we investigated the cellular mechanism by which CARD9 controls pathogenic Th17 responses and the onset of disease in both experimental murine AS and patients.

Methods

Experiments in SKG, Card9^-/-SKG, neutrophil-deplete SKG mice along with in vitro murine, neutrophil and CD4⁺ T cell cocultures examined Card9 function in neutrophil activation, Th17 induction and arthritis in experimental AS. In AS patients the neutrophil: Bath Ankylosing Spondylitis Functional Index relationship was analysed. In vitro studies with autologous neutrophil: T cell cocultures examined endogenous CARD9 versus the AS-associated variant (

SUBMITTER: Rosenzweig HL 

PROVIDER: S-EPMC10850635 | biostudies-literature | 2024 Jan

REPOSITORIES: biostudies-literature