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Influence of 1,25-dihydroxy vitamin D3 on TLR4-induced activation of antigen presenting cells is dependent on the order of receptor engagement.
MedLine Citation:
PMID:  21529994     Owner:  NLM     Status:  Publisher    
Abstract/OtherAbstract:
The vitamin D metabolite, 1,25-(OH)(2)D(3), binds the vitamin D receptor (VDR) to exert its regulatory effects at the transcription level. VDR is expressed in professional antigen-presenting cells (pAPCs), such as macrophages (Mø) and dendritic cells (DCs). We show for the first time that the 24-hydroxylase enzyme is activated in bone marrow-derived dendritic cell (BMDC), due to 1,25(OH)(2)D(3) stimulation which resulted in the induction of its gene, CYP24A1. Furthermore, we provide evidence that the influence of 1,25-(OH)(2)D(3) on TLR-4-L-induced activation of pAPC is dependent on the order of VDR and TLR-4 engagement. Thus, pre-treatment of pAPC with 1,25-(OH)(2)D(3) partially inhibited LPS-induced nitric oxide (NO) production. However, these inhibitory effects were not observed when LPS and 1,25-(OH)(2)D(3) were added simultaneously or when LPS preceded 1,25-(OH)(2)D(3). Moreover, we found that 1,25-(OH)(2)D(3) pre-treatment of pAPCs did not cause general suppression since it interfered with NO levels but not with the cytokines IL-6 or TNF-α. Consequently, engagement of VDR by 1,25-(OH)(2)D(3) can partially interfere with TLR-4-L-induced activation of pAPCs only when it occurs before TLR-4 stimulation.
Authors:
Vandana Gambhir; Julia Kim; Sarah Siddiqui; Michelle Taylor; Valarie Byford; Elaine O Petrof; Glenville Jones; Sameh Basta
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Publication Detail:
Type:  JOURNAL ARTICLE     Date:  2011-4-7
Journal Detail:
Title:  Immunobiology     Volume:  -     ISSN:  1878-3279     ISO Abbreviation:  -     Publication Date:  2011 Apr 
Date Detail:
Created Date:  2011-5-2     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  8002742     Medline TA:  Immunobiology     Country:  -    
Other Details:
Languages:  ENG     Pagination:  -     Citation Subset:  -    
Copyright Information:
Copyright © 2011. Published by Elsevier GmbH.
Affiliation:
Department of Microbiology and Immunology, Queen's University, Kingston, Ontario, Canada.
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