15. Neutrophils in GCA

Résumé fourni par la source

The role of neutrophils, if any, in GCA has rarely been studied. Herein we monitored neutrophil markers of activation and reactivity onto an endothelial monolayers, making comparisons across diseases and during GCA clinical management with a canonical glucocorticoid dose regimen over a 6-month period. Blood samples were taken from over 12 patients in total (mean age 72 ± 2 years) within 48 h of therapy beginning and at weeks 1, 4 and 24 post-glucocorticoid; these were compared with samples obtained from OA patients (n = 10; mean age 70 ± 3 years). A ‘mixed’ high steroid group was also included (n = 6; 47 ± 10 years old). FACS revealed three distinct neutrophils populations and phenotypes. Within 48 h of steroid treatment, neutrophils had a CD62LloCD11bhi phenotype, whereas week 1 neutrophils were CD62LloCD11blo and displayed minimal adhesion to endothelial monolayers under flow. At week 24 (i.e. lowest glucocorticoid dose) neutrophils were CD62LhiCD11bhi with increased endothelial adhesion under flow. Week 24 plasma analyses showed high levels of IL-17 and IL-6. Importantly, comparison of week 1 and 24 samples revealed a suppressive neutrophil effect on T-cell proliferation at the former time point only. These changes were not seen in the other two groups, OA and patients on high steroid therapy. Collectively, these data support the notion that GCA may be incompletely controlled by glucocorticoid therapy, since tapering leads to loss of the neutrophil suppressor subset. This may lead to disease relapse with higher risk of vascular complications. We propose monitoring neutrophil phenotype might inform on GCA disease status, predict risk of relapse and facilitate steroid tapering in individual patient. Funding: Supported by the British Heart Foundation (PG/09/060).

Ce résumé expose les affirmations des auteurs. BNTIC ne l’interprète pas comme une validation indépendante des résultats.