Receptors, Calcitriol

Publication Title: 
Journal of the National Cancer Institute

BACKGROUND: 1,25-Dihydroxyvitamin D(3) inhibits growth of several types of human cancer cells in vitro, but its therapeutic use is hampered because it causes hypercalcemia. 19-nor-1,25-Dihydroxyvitamin D(2) (paricalcitol) is a noncalcemic vitamin D analog that is approved by the Food and Drug Administration for the treatment of secondary hyperparathyroidism. We investigated the antitumor activity and mechanism of action of paricalcitol in vitro and in vivo. METHODS: Effects of paricalcitol on proliferation, the cell cycle, differentiation, and apoptosis were examined in cancer cell lines.

Author(s): 
Kumagai, Takashi
O'Kelly, James
Said, Jonathan W.
Koeffler, H. Phillip
Publication Title: 
Blood

Insulin-like growth factor binding protein-3 (IGFBP-3) can cause growth suppressive and proapoptotic effects on retinoids in many types of cancer cells. However, the expression and effects of IGFBP-3 in myeloid leukemia cells have not been elucidated. In this study, we found no IGFBP-3 expression in the human myeloid leukemia cell lines either at baseline or after stimulation with all-trans retinoic acid (ATRA). Human recombinant IGFBP-3 induced growth arrest and apoptosis of HL-60 and NB4 cells.

Author(s): 
Ikezoe, Takayuki
Tanosaki, Sakae
Krug, Utz
Liu, Bingrong
Cohen, Pinchas
Taguchi, Hirokuni
Koeffler, H. Phillip
Publication Title: 
Archives of Biochemistry and Biophysics

Mice lacking the vitamin D receptor (VDR) are resistant to airway inflammation. Pathogenic immune cells capable of transferring experimental airway inflammation to wildtype (WT) mice are present and primed in the VDR KO mice. Furthermore, the VDR KO immune cells homed to the WT lung in sufficient numbers to induce symptoms of asthma. Conversely, WT splenocytes, Th2 cells and hematopoetic cells induced some symptoms of experimental asthma when transferred to VDR KO mice, but the severity was less than that seen in the WT controls.

Author(s): 
Wittke, Anja
Chang, Andrew
Froicu, Monica
Harandi, Omid F.
Weaver, Veronika
August, Avery
Paulson, Robert F.
Cantorna, Margherita T.
Publication Title: 
Proceedings of the National Academy of Sciences of the United States of America

CD1d-reactive natural killer T (NKT) cells with an invariant T cell receptor Valpha14 rearrangement are a unique subset of lymphocytes, which play important roles in immune regulation, tumor surveillance, and host defense against pathogens. Vitamin D is a nutrient/hormone that has been shown to regulate conventional T cell responses but not T cell development. The data show that expression of the vitamin D receptor (VDR) is required for normal development and function of iNKT cells. The iNKT cells from VDR KO mice are intrinsically defective and lack T-bet expression.

Author(s): 
Yu, Sanhong
Cantorna, Margherita T.
Publication Title: 
International Immunology

1,25-dihydroxyvitamin D(3) [1,25(OH)(2)D(3)] and the vitamin D receptor (VDR) are important regulators of autoimmunity. The effect of the VDR on the ability of mice to fight a primary or secondary infection has not been determined. Young and old VDR knockout (KO) mice were able to clear both primary and secondary infections with Listeria monocytogenes. However, the kinetics of clearance was somewhat delayed in the absence of the VDR.

Author(s): 
Bruce, Danny
Whitcomb, James P.
August, Avery
McDowell, Mary Ann
Cantorna, Margherita T.
Publication Title: 
Proceedings of the National Academy of Sciences of the United States of America

Specific pathogen-free IL-10 KO mice failed to develop inflammatory bowel disease (IBD), whereas IL-10/vitamin D receptor (VDR) double KO mice developed fulminating IBD. WT CD4 T cells inhibited experimental IBD, while VDR KO CD4 T cells failed to suppress IBD. VDR KO mice had normal numbers and functions of regulatory T cells. The percentages of IL-17- and IFN-gamma-secreting T cells in the gut of mice reconstituted with WT and VDR KO CD4 T cells were also not different.

Author(s): 
Yu, Sanhong
Bruce, Danny
Froicu, Monica
Weaver, Veronika
Cantorna, Margherita T.
Publication Title: 
The Proceedings of the Nutrition Society

Vitamin D and the vitamin D receptor (VDR) have been shown to be important regulators of the immune system. In particular, vitamin D and VDR deficiency exacerbates experimental autoimmune diseases such as inflammatory bowel disease (IBD). IBD develops due to an immune-mediated attack by pathogenic T-cells that overproduce IL-17 and IFN-gamma and a few regulatory cells. VDR knockout mice have twice as many T-cells making IL-17 and IFN-gamma than wild-type mice.

Author(s): 
Cantorna, Margherita T.
Publication Title: 
Annals of the New York Academy of Sciences

Vitamin D is an important regulator of immune function. T cells express the vitamin D receptor (VDR) and have been shown to be direct and indirect vitamin D targets. Why should T cells be responsive to vitamin D? The data suggest that expression of the VDR is required for the development of two cell types, NKT cells and CD8αα T cells, which inhibit autoimmunity. In addition, effector T cell cytokine production is regulated by vitamin D.

Author(s): 
Cantorna, Margherita T.
Publication Title: 
Journal of Immunology (Baltimore, Md.: 1950)

Vitamin D and vitamin D receptor (VDR) deficiency results in severe symptoms of experimental inflammatory bowel disease in several different models. The intraepithelial lymphocytes of the small intestine contain large numbers of CD8αα(+) T cells that have been shown to suppress the immune response to Ags found there. In this study, we determined the role of the VDR in the development of CD8αα(+) T cells. There are fewer total numbers of TCRαβ(+) T cells in the gut of VDR knockout (KO) mice, and that reduction was largely in the CD8αα(+) TCRαβ(+) cells.

Author(s): 
Bruce, Danny
Cantorna, Margherita T.
Publication Title: 
International Immunology

Multiple pathways converge to result in the overexpression of T(h)17 cells in the absence of either vitamin D or the vitamin D receptor (VDR). CD4(+) T cells from VDR knockout (KO) mice have a more activated phenotype than their wild-type (WT) counterparts and readily develop into T(h)17 cells under a variety of in vitro conditions. Vitamin D-deficient CD4(+) T cells also overproduced IL-17 in vitro and 1,25 dihydroxyvitamin D(3) inhibited the development of T(h)17 cells in CD4(+) T-cell cultures.

Author(s): 
Bruce, Danny
Yu, Sanhong
Ooi, Jot Hui
Cantorna, Margherita T.

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