BACKGROUND: B cells have recently entered the stage as an important accessory player in type 1 diabetes (T1D) etiopathogenesis. Experimental studies suggest regulatory functions of vitamin D on B cells. However, only a few human studies, with considerable methodological limitations, have been conducted within this field.

OBJECTIVE: Our objective was to investigate if higher 25-hydroxyvitamin D (25(OH)D) concentrations were inversely associated with β-cell autoantigens glutamic acid decarboxylase (isoform 65) (GADA) and insulinoma associated antigen-2A (IA-2A). Further, we also wanted to examine the relationship between 25(OH)D and total antibody concentrations.

METHODS: We randomly selected 500 patients with newly diagnosed T1D and 500 siblings for 25(OH)D, antibody and genetic analysis from the population-based Danish Registry of Childhood and Adolescent Diabetes. The relative change (RC) in the mean concentration of GADA, IA-2A and antibody isotypes by a 10 nmol/L increase in 25(OH)D concentration was modeled by a robust log-normal model regression.

RESULTS: We found no association between either 25(OH)D and GADA [adjusted RC per 10 nmol/L increase: 1.00; 95% confidence interval (CI): 0.98-1.02] or IA-2A [adjusted RC per 10 nmol/L increase: 0.92; CI: 0.76-1.12]. Further, 25(OH)D was not associated total concentration of antibody isotypes (immunoglobulin (Ig)A, IgE, IgG and IgM). All null findings were unaltered after adjustment for genetic variation in the vitamin D pathway.

CONCLUSION: Physiological concentrations of 25(OH)D are unlikely to have a clinically important effect on antibody concentrations in a pediatric population of newly diagnosed patients with T1D and their healthy siblings. This article is protected by copyright. All rights reserved.