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293 Effect of high dose cholecalciferol during sle flares in mir-146a expression, regulatory t-cells and il-17a expression
  1. A Marinho1,
  2. C Carvalho2,
  3. D Boleixa2,
  4. A Bettencourt2,
  5. B Martins da Silva2 and
  6. C Vasconcelos1
  1. 1Centro Hospitalar Do Porto, Internal Medicine, Porto, Portugal
  2. 2ICBAS, Immunogenetics, Porto, Portugal

Abstract

Background and aims A few microRNAs have known gene expression regulatory roles in innate immunity. The miR-146a, seems to be a negative regulator of innate immunity. Interestingly, miR-146a has been reported to be downregulated in PBMCs of SLE patients, being negatively correlated with clinical disease activity and with IFN levels. The ability of vitamin D to regulate miRs and their emerging relationship have been proposed through several experimental approaches. The aim of this study was to determine the Vitamin D effect in miR-146a expression and in T-Reg and TCD4+ IL-17A producing cells, in SLE.

Methods An interventional study with 3 weeks follow-up of SLE patients with a high dose vitamin D supplementation (50.000 UI or 100.000 UI/Week) was done. We assessed four female patients who had a SLEDAI >6 and at least one BILAG A. At screening, relevant data were compiled: SLEDAI-2K, BILAG score, concomitant therapy, previous SLE manifestations, 25(OH)D levels, T-Reg/IL-17A ratio and miR-146a expression. At Week 3: 25(OH) D levels, T-Reg/IL-17A+ ratio, miR-146a expression, SLEDAI 2 K, BILAG and concomitant therapy.

Results No significant difference were found, regarding Vitamin D levels, before and after supplementation. Regarding Tregs/IL-17A ratio before and after supplementation, no benefits, regarding enhancing of T-regs or decrease of Il 17-A producing cells. No significative differences were found in miR-146a expression between controls and SLE active patients before and after vitamin D supplementation.

Conclusions Severe SLE activity may cause resistance to Vitamin D therapeutical effects, including enhancing of Vitamin D levels and immunogenetic effects.

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