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. 
Our objective was to investigate whether 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. 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 modelled by a 
robust log-normal regression model. We found no association between 25(OH)D and 
GADA [adjusted RC per 10 nmol/l increase: 1.00; 95% confidence interval (CI): 
0.98-1.02] and IA-2A [adjusted RC per 10 nmol/l increase: 0.92; CI: 0.76-1.12]. 
Further, 25(OH)D was not associated with the 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. 
Physiological concentrations of 25(OH)D are unlikely to have a clinically 
important effect on antibody concentrations in a paediatric population of newly 
diagnosed patients with T1D and their healthy siblings.