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This Article Full Text Full Text (PDF) All Versions of this Article: JOE-08-0170v1 198/2/261    most recent Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Web of Science (2) Citing Articles via Google Scholar Google Scholar Articles by Chun, R. F Articles by Hewison, M. Search for Related Content PubMed PubMed Citation Articles by Chun, R. F Articles by Hewison, M.

¹ Department of Orthopaedic Surgery, David Geffen School of Medicine, UCLA, 615 Charles E Young Drive South, Los Angeles, California 90095, USA² Molecular Biology Institute, UCLA, Los Angeles, California 90095, USA

(Correspondence should be addressed to M Hewison; Email: mhewison{at}mednet.ucla.edu)

Our perception of the vitamin D system continues to evolve. Recent studies have re-evaluated the parameters for adequate vitamin D status in humans, revealing a high prevalence of insufficiency in many populations throughout the world. Other reports have highlighted the potential consequences of vitamin D insufficiency beyond established effects on bone homeostasis. Most notably, there is now strong evidence of a role for vitamin D in modulating innate and adaptive immunities, with insufficiency being linked to infectious disease and other immune disorders. To date, signaling pathways for these new responses to vitamin D have been based on established endocrine models for active 1,25-dihydroxyvitamin D, despite present evidence for more localized, intracrine modes of action. In the following review, we provide a fresh perspective on vitamin D signaling in non-classical target cells such as macrophages by highlighting novel factors associated with the transport and action of this pluripotent secosteroid.

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