Restoration of regulatory and effector T cell balance and B cell homeostasis in systemic lupus erythematosus patients through vitamin D supplementation.
BACKGROUND
Systemic lupus erythematosus (SLE) is a T and B cell-dependent autoimmune disease characterized by the appearance of autoantibodies, a global regulatory T cells (Tregs) depletion and an increase in Th17 cells. Recent studies have shown the multifaceted immunomodulatory effects of vitamin D, notably the expansion of Tregs and the decrease of Th1 and Th17 cells. A significant correlation between higher disease activity and lower serum 25-hydroxyvitamin D levels [25(OH)D] was also shown.


METHODS
In this prospective study, we evaluated the safety and the immunological effects of vitamin D supplementation (100,000 IU of cholecalciferol per week for 4 weeks, followed by 100,000 IU of cholecalciferol per month for 6 months.) in 20 SLE patients with hypovitaminosis D.


RESULTS
Serum 25(OH)D levels dramatically increased under vitamin D supplementation from 18.7±6.7 at day 0 to 51.4±14.1 (p<0.001) at 2 months and 41.5±10.1 ng/mL (p<0.001) at 6 months. Vitamin D was well tolerated and induced a preferential increase of naïve CD4+ T cells, an increase of regulatory T cells and a decrease of effector Th1 and Th17 cells. Vitamin D also induced a decrease of memory B cells and anti-DNA antibodies. No modification of the prednisone dosage or initiation of new immunosuppressant agents was needed in all patients. We did not observe SLE flare during the 6 months follow-up period.


CONCLUSIONS
This preliminary study suggests the beneficial role of vitamin D in SLE patients and needs to be confirmed in randomized controlled trials.
Benjamin
B
Terrier
Nicolas
N
Derian
Yoland
Y
Schoindre
Wahiba
W
Chaara
Guillaume
G
Geri
Noël
N
Zahr
Kubéraka
K
Mariampillai
Michelle
M
Rosenzwajg
Wassila
W
Carpentier
Lucile
L
Musset
Jean-Charles
JC
Piette
Adrien
A
Six
David
D
Klatzmann
David
D
Saadoun
Cacoub
C
Patrice
Nathalie
N
Costedoat-Chalumeau
D000328:Adult; D000888:Antibodies, Anti-Idiotypic / Q000097:blood; D001402:B-Lymphocytes / Q000187:drug effects / Q000473:pathology*; D002762:Cholecalciferol / Q000008:administration & dosage / Q000494:pharmacology / Q000627:therapeutic use; D015897:Comorbidity; D004247:DNA / Q000276:immunology; D019587:Dietary Supplements; D004305:Dose-Response Relationship, Drug; D005260:Female; D005500:Follow-Up Studies; D006706:Homeostasis / Q000187:drug effects*; D006801:Humans; D008137:Longitudinal Studies; D008180:Lupus Erythematosus, Systemic / Q000097:blood / Q000453:epidemiology / Q000473:pathology*; D011446:Prospective Studies; D013601:T-Lymphocytes / Q000187:drug effects / Q000473:pathology*; D050378:T-Lymphocytes, Regulatory / Q000187:drug effects / Q000473:pathology; D018417:Th1 Cells / Q000187:drug effects / Q000473:pathology; D058504:Th17 Cells / Q000187:drug effects / Q000473:pathology; D014807:Vitamin D / Q000008:administration & dosage* / Q000031:analogs & derivatives / Q000097:blood / Q000494:pharmacology* / Q000627:therapeutic use; D014808:Vitamin D Deficiency / Q000097:blood / Q000188:drug therapy / Q000453:epidemiology
D000888:Antibodies, Anti-Idiotypic; D014807:Vitamin D; D002762:Cholecalciferol; D004247:DNA; C104450:25-hydroxyvitamin D