Studie
NAD+ augmentation by nicotinamide riboside engages SLIT2/ROBO1 signaling to attenuate Th17 inflammation in psoriasis.
In psoriasis, 4 weeks of nicotinamide riboside altered Th17 signalling; the abstract gives no N or clinical outcome.
Den placebokontrollerade studien undersökte nicotinamide riboside (NR) hos personer med mild till måttlig psoriasis. Deltagarna fick NR 500 mg via munnen två gånger dagligen eller matchande placebo i 4 veckor. Blodprov togs före och efter perioden med tillskott. The abstract does not report the participant number, allocation numbers, a clinical psoriasis score, or symptom results. Instead, its central outcome is immune target engagement. NR reduced Th17 immune responsiveness, and bulk CD4+ T-cell RNA sequencing identified induction of the SLIT-ROBO signalling pathway. Circulating SLIT2 increased after NR supplementation, and the abstract reports increased SLIT2 production in dermal fibroblasts. Pharmacological and genetic experiments in CD4+ T cells and fibroblasts implicated SLIT2 acting through ROBO1, with inhibition of Rho GTPase signalling, reduced canonical Th17 polarisation, and reduced inflammatory activation in fibroblasts. These findings are mechanistic and disease-specific. They do not establish an improvement in psoriasis symptoms, clinical outcomes, or ageing-related outcomes. The funding listed is the NHLBI Division of Intramural Research. A four-week immunology study cannot support broad claims about NAD augmentation for longevity.
NAD+ augmentation had anti-inflammatory effects in psoriasis through SLIT2-ROBO1-mediated crosstalk that suppressed Th17-driven inflammation.
The abstract does not state N and reports no clinical psoriasis endpoint. Follow-up was four weeks, and the main findings are mechanistic immune markers in a psoriasis population.
Citerad av
1 encyklopediartiklar refererar till denna studie.