Contributions
Abstract: P627
Type: Poster
Abstract Category: Therapy - disease modifying - Immunomodulation/Immunosuppression
Multiple sclerosis (MS) is characterized by a disturbed immune homeostasis and low serum vitamin D levels are associated with an increased disease activity. While vitamin D has been hypothesized to promote the maintenance of immune homeostasis, vitamin D3 supplementation could be of benefit to patients with MS. We investigated the immune regulatory effects of high dose vitamin D3 supplementation in the SOLARIUM study.
Thirty Dutch relapsing remitting (RR)MS patients treated with IFNβ-1a received high dose vitamin D3 supplementation and 23 patients received placebo during a period of 48 weeks. Lymphocytes were characterized by flow cytometry and in vitro cytokine secretion was assessed in the presence or absence of 1,25(OH)2D3 using Luminex technology.
The proportion of cells in the regulatory immune cell compartment (nTreg, iTreg and Breg) was not altered upon vitamin D3 supplementation. Proportions of T helper subsets were not affected by vitamin D3, except for the proportion of IL4+ Th cells, which decreased in the placebo but not in the vitamin D3 group. T cell cytokine secretion increased, most pronounced for IL5 and latency activated protein of TGFβ, in the placebo group but not in the vitamin D3 group. Lymphocytes remained equally reactive to in vitro 1,25(OH)2D3.
In conclusion, high dose vitamin D3 supplementation did not result in a relative increase in lymphocytes with a regulatory phenotype. However, this study supports the hypothesis that vitamin D contributes to the maintenance of immune homeostasis by preventing further disturbance of the T cell compartment early in the disease course of MS.
SOLARIUM study group: Prof. Dr. R. Hupperts, Zuyderland Medical Center, Sittard; Drs. J. Samijn, Maasstad Hospital, Rotterdam; Dr. F. Verheul, Groene Hart Hospital, Gouda; Dr. S. Frequin, St. Antonius Hospital, Nieuwegein, the Netherlands.
Disclosure:
AM, JS, LR, MT and JD report no disclosures.
RH received honoraria for lectures and advisory boards and Research Grants from Merck, Biogen, Sanofi-Genzyme, Novartis and TEVA. This study was financially supported by Merck KGaA (Darmstadt, Germany) and the Nationaal MS Fonds (the Netherlands)
Abstract: P627
Type: Poster
Abstract Category: Therapy - disease modifying - Immunomodulation/Immunosuppression
Multiple sclerosis (MS) is characterized by a disturbed immune homeostasis and low serum vitamin D levels are associated with an increased disease activity. While vitamin D has been hypothesized to promote the maintenance of immune homeostasis, vitamin D3 supplementation could be of benefit to patients with MS. We investigated the immune regulatory effects of high dose vitamin D3 supplementation in the SOLARIUM study.
Thirty Dutch relapsing remitting (RR)MS patients treated with IFNβ-1a received high dose vitamin D3 supplementation and 23 patients received placebo during a period of 48 weeks. Lymphocytes were characterized by flow cytometry and in vitro cytokine secretion was assessed in the presence or absence of 1,25(OH)2D3 using Luminex technology.
The proportion of cells in the regulatory immune cell compartment (nTreg, iTreg and Breg) was not altered upon vitamin D3 supplementation. Proportions of T helper subsets were not affected by vitamin D3, except for the proportion of IL4+ Th cells, which decreased in the placebo but not in the vitamin D3 group. T cell cytokine secretion increased, most pronounced for IL5 and latency activated protein of TGFβ, in the placebo group but not in the vitamin D3 group. Lymphocytes remained equally reactive to in vitro 1,25(OH)2D3.
In conclusion, high dose vitamin D3 supplementation did not result in a relative increase in lymphocytes with a regulatory phenotype. However, this study supports the hypothesis that vitamin D contributes to the maintenance of immune homeostasis by preventing further disturbance of the T cell compartment early in the disease course of MS.
SOLARIUM study group: Prof. Dr. R. Hupperts, Zuyderland Medical Center, Sittard; Drs. J. Samijn, Maasstad Hospital, Rotterdam; Dr. F. Verheul, Groene Hart Hospital, Gouda; Dr. S. Frequin, St. Antonius Hospital, Nieuwegein, the Netherlands.
Disclosure:
AM, JS, LR, MT and JD report no disclosures.
RH received honoraria for lectures and advisory boards and Research Grants from Merck, Biogen, Sanofi-Genzyme, Novartis and TEVA. This study was financially supported by Merck KGaA (Darmstadt, Germany) and the Nationaal MS Fonds (the Netherlands)