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1,25‐Dihydroxyvitamin D 3 Alters the Profile of Bone Marrow‐Derived Dendritic Cells of NOD Mice
Author(s) -
ETTEN EVELYNE,
DARDENNE OLIVIER,
GYSEMANS CONNY,
OVERBERGH LUT,
MATHIEU CHANTAL
Publication year - 2004
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1196/annals.1337.030
Subject(s) - nod , bone marrow , chemistry , microbiology and biotechnology , nod mice , immunology , biology , biochemistry , gene
A bstract : 1,25‐dihydroxyvitamin D 3 [1,25(OH) 2 D 3 ] prevents autoimmune diabetes in nonobese diabetic (NOD) mice. A major target for 1,25(OH) 2 D 3 in the immune system is the dendritic cell (DC). Since important DC abnormalities have been described in NOD mice, we investigated the effects of 1,25(OH) 2 D 3 on the yield and phenotype of DCs generated from bone marrow of NOD mice compared to control congenic nonobese diabetes‐resistant (NOR) mice. In both mouse strains, exposure of the bone marrow‐derived cells to 1,25(OH) 2 D 3 increased the proportion of CD11c + DCs after culture. Surface expression of MHC II, CD86, and CD54 on NOR‐derived DCs was decreased after 1,25(OH) 2 D 3 treatment, while CD40 remained unchanged. On NOD‐derived DCs, 1,25(OH) 2 D 3 only inhibited the expression of MHC II and CD86. 1,25(OH) 2 D 3 inhibited IL‐12 and IL‐10 secretion after IFNγ and LPS stimulation. In vitro treatment with 1,25(OH) 2 D 3 alters DC yield from bone marrow cultures and alters the phenotype of the cells in NOD as well as in NOR mice. NOD‐derived DCs were more resistant to the 1,25(OH) 2 D 3 effects than were NOR‐derived DCs.