Topical 1,25‐dihydroxyvitamin D<sub>3</sub> subverts the priming ability of draining lymph node dendritic cells

Gorman, Shelley; Judge, Melinda A.; Hart, Prue H.

doi:10.1111/j.1365-2567.2010.03315.x

Cited by 37 publications

(42 citation statements)

References 33 publications

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“…The mean fluorescence intensity values from multiple experiments for these activation markers on DCs in SDLNs are shown in Table II. As expected, activation marker expression was significantly increased on migratory FITC hi DCs (32,33). Similar to the results described above (Fig.…”

Section: Expression Of Activation Markers For T Cells Is Not Reduced supporting

confidence: 80%

Altered Immunity and Dendritic Cell Activity in the Periphery of Mice after Long-Term Engraftment with Bone Marrow from Ultraviolet-Irradiated Mice

Scott

Strickland

et al. 2013

The Journal of Immunology

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Alterations to dendritic cell (DC) progenitors in the bone marrow (BM) may contribute to long-lasting systemic immunosuppression (>28 d) following exposure of the skin of mice to erythemal UV radiation (UVR). DCs differentiated in vitro from the BM of mice 3 d after UVR (8 kJ/m2) have a reduced capacity to initiate immunity (both skin and airways) when adoptively transferred into naive mice. Studies in IL-10−/− mice suggested that UV-induced IL-10 was not significantly involved. To investigate the immune capabilities of peripheral tissue DCs generated in vivo from the BM of UV-irradiated mice, chimeric mice were established. Sixteen weeks after reconstitution, contact hypersensitivity responses were significantly reduced in mice reconstituted with BM from UV-irradiated mice (UV-chimeric). When the dorsal skin of UV-chimeric mice was challenged with innate inflammatory agents, the hypertrophy induced in the draining lymph nodes was minimal and significantly less than that measured in control-chimeric mice challenged with the same inflammatory agent. When DCs were differentiated from the BM of UV-chimeric mice using FLT3 ligand or GM-CSF + IL-4, the cells maintained a reduced priming ability. The diminished responses in UV-chimeric mice were not due to different numerical or proportional reconstitution of BM or the hematopoietic cells in blood, lymph nodes, and skin. Erythemal UVR may imprint a long-lasting epigenetic effect on DC progenitors in the BM and alter the function of their terminally differentiated progeny.

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Section: Expression Of Activation Markers For T Cells Is Not Reduced supporting

confidence: 80%

Altered Immunity and Dendritic Cell Activity in the Periphery of Mice after Long-Term Engraftment with Bone Marrow from Ultraviolet-Irradiated Mice

Scott

Strickland

et al. 2013

The Journal of Immunology

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“…11,34,[38][39][40][41] Topical treatment with vitamin D has been shown to decrease the allo-stimulatory capacity of DCs in the skindraining lymph nodes, and enhanced the suppressive capacity of regulatory T cells. 42 The growing in vitro and animal literature demonstrating the effects of vitamin D on DC and T-cell populations support the hypothesis that vitamin D has a role in modulating GVHD.…”

Section: Discussionmentioning

confidence: 92%

Low levels of 25-hydroxyvitamin D before allogeneic hematopoietic SCT correlate with the development of chronic GVHD

Glotzbecker

Aldridge

et al. 2012

Bone Marrow Transplant

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Vitamin D, a hormone involved in bone and calcium homeostasis, has been shown to have potent immunomodulatory effects. We performed a retrospective cohort analysis to evaluate whether monohydroxyvitamin D levels before allogeneic hematopoietic SCT (HSCT) correlate with the risk of GVHD. Fifty-three patients who underwent myeloablative HSCT were studied. Vitamin D levels were measured in serum samples obtained before HSCT. The median 25-hydroxyvitamin vitamin D level was 21.9 ng/mL (7.8-45.7). The cumulative incidence (CI) of grades II-IV acute GVHD at 100 days was 53.1% in patients with vitamin Do25, versus 33.3% in patients with vitamin DX25 ng/mL (P ¼ 0.13). The CI of chronic GVHD (cGVHD) at 2 years in patients with vitamin Do25 was 63.8%, compared with 23.8% in patients with vitamin DX25 ng/mL (P ¼ 0.009). Similarly, the 2 year CI of extensive cGVHD was significantly greater in patients with vitamin Do25 compared with those with vitamin DX25 ng/mL (54.5% versus 14.3%, P ¼ 0.005). In a multivariable competing risk model, low pre-transplant vitamin D levels remained a significant factor associated with cGVHD (hazard ratio ¼ 5.26, P ¼ 0.02). Our results demonstrate that vitamin D deficiency before HSCT is associated with an increased risk of cGVHD. (2013) 48, 593-597; doi:10.1038/bmt.2012 published online 24 September 2012 Keywords: Vitamin D; GVHD; hematopoietic SCT INTRODUCTION GVHD remains a significant cause of morbidity and mortality following allogeneic HSCT. Despite standard immune-suppression with a calcineurin inhibitor and MTX, grade II-IV acute GVHD rates range from 20-50% and chronic GVHD from 40-50% after BMT. Bone Marrow Transplantation

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“…Nevertheless, our observations that the hazard ratio for ACR increased from 3.3 observed in the entire group of vitamin D deficient patients to 4.4 in the subset of vitamin D deficient not treated with 1,25(OH) 2 D3 and the hazard ratio decreased to 1.5 in the subset of vitamin D deficient treated with 1,25(OH) 2 D3 is in accord with vitamin D deficiency being a risk factor for ACR and consistent with experimental evidence that 1,25(OH) 2 D3 prolongs allograft survival in a number of experimental models of transplantation (2–5). Possible mechanisms for the allograft protective role of 1,25(OH) 2 D3 include: decreasing T cell production of inflammatory mediators such as IL-2 and interferon-γ (6, 7), downregulating the immunogenic activity of dendritic cells activity (20), and upregulating the immunoprotective activity of T regulatory cells (9, 10). …”

Section: Discussionmentioning

confidence: 99%

“…In a randomized controlled trial of 19 recipients of living donor kidney grafts, calcitriol treatment of kidney donors and recipients was associated with an increased percentage of CD3+CD4+CD25+ cells in peripheral blood compared to the untreated group (9). Application of 1,25(OH) 2 D3 to the skin of mice is associated with alterations in the phenotype of CD11c+ dendritic cells and enhanced regulatory activity of CD4+CD25+ cells in draining lymph nodes (10). …”

Section: Introductionmentioning

confidence: 99%

Circulating Levels of 25-Hydroxyvitamin D and Acute Cellular Rejection in Kidney Allograft Recipients

et al. 2014

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Background Vitamin D, in addition to its established role in bone metabolism, may regulate the immune system and impact the outcome of allografts. Methods We identified 351 kidney allograft recipients who had serum levels of 25-hydroxyvitamin D (25[OH]D) measured within the first 30 days of transplantation. We evaluated the relationship between the circulating levels of 25(OH)D and acute cellular rejection (ACR), CMV disease, BKV nephropathy (BKVN), and kidney graft function. Results Vitamin D deficiency (circulating levels of 25(OH)D ≤20 ng/mL, defined using The Endocrine Society Clinical Practice 2011 Guideline) was observed in 216 (61.5%) of 351 kidney graft recipients. Vitamin D deficiency was more frequent in female recipients (P=0.007, Fisher’s Exact test) and African American recipients (P<0.001) and was less frequent in preemptive kidney graft recipients (P=0.002). Biopsy-confirmed ACR was more frequent in the vitamin D deficient group than in the sufficient group (10.2% vs. 3.7%, P=0.04). By multivariable Cox regression analysis, vitamin D deficiency was an independent risk factor for ACR (Hazard Ratio: 3.3, P=0.02). Vitamin D deficiency was not associated with CMV disease, BKVN, or kidney allograft function at 1 year. 1,25-dihydroxyvitamin D3 supplementation initiated within the first 90 days of transplantation was associated with a lesser incidence of ACR compared to no treatment with 1,25-dihydroxyvitamin D3 (5.1% vs. 13.0%, P=0.099). Conclusions Vitamin D deficiency is an independent risk factor for development of ACR within the first year of kidney transplantation and 1,25-dihydroxyvitamin D3 supplementation may help reduce the occurrence of ACR in the vitamin D deficient group.

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Topical 1,25‐dihydroxyvitamin D₃ subverts the priming ability of draining lymph node dendritic cells

Abstract: Interest in the involvement of vitamin D in various body systems and disease settings has recently increased with observations that deficiency in this hormone is an emerging health problem in many countries. With ultraviolet B (UVB) irradiation

Cited by 37 publications

References 33 publications

Altered Immunity and Dendritic Cell Activity in the Periphery of Mice after Long-Term Engraftment with Bone Marrow from Ultraviolet-Irradiated Mice

Altered Immunity and Dendritic Cell Activity in the Periphery of Mice after Long-Term Engraftment with Bone Marrow from Ultraviolet-Irradiated Mice

Low levels of 25-hydroxyvitamin D before allogeneic hematopoietic SCT correlate with the development of chronic GVHD

Circulating Levels of 25-Hydroxyvitamin D and Acute Cellular Rejection in Kidney Allograft Recipients

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Topical 1,25‐dihydroxyvitamin D3 subverts the priming ability of draining lymph node dendritic cells

Abstract: Interest in the involvement of vitamin D in various body systems and disease settings has recently increased with observations that deficiency in this hormone is an emerging health problem in many countries. With ultraviolet B (UVB) irradiation

Cited by 37 publications

References 33 publications

Altered Immunity and Dendritic Cell Activity in the Periphery of Mice after Long-Term Engraftment with Bone Marrow from Ultraviolet-Irradiated Mice

Altered Immunity and Dendritic Cell Activity in the Periphery of Mice after Long-Term Engraftment with Bone Marrow from Ultraviolet-Irradiated Mice

Low levels of 25-hydroxyvitamin D before allogeneic hematopoietic SCT correlate with the development of chronic GVHD

Circulating Levels of 25-Hydroxyvitamin D and Acute Cellular Rejection in Kidney Allograft Recipients

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Topical 1,25‐dihydroxyvitamin D₃ subverts the priming ability of draining lymph node dendritic cells