Vitamin D immunoregulation through dendritic cells

Bscheider, Michael; Butcher, Eugene C.

doi:10.1111/imm.12610

Cited by 99 publications

(67 citation statements)

References 81 publications

(190 reference statements)

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“…The DCs can then traffic to the mesenteric lymph node and modulate effector T cell function, or can act more locally to promote airway inflammation (19). Whereas UPM has been reported to promote the maturation of DCs (19), vitamin D has been shown independently to have the opposite effect, acting to promote a tolerogenic DC phenotype (20). Within the lung, memory CD4 1 T cells are extremely abundant and therefore any modulation of these cells by UPM-primed DCs may play an important role in air pollution-induced disease exacerbations (21), an issue that we sought to address in the current study.…”

Section: Clinical Relevancementioning

confidence: 99%

Vitamin D Counteracts an IL-23–Dependent IL-17A⁺IFN-γ⁺ Response Driven by Urban Particulate Matter

Mann

Pfeffer

et al. 2017

Am J Respir Cell Mol Biol

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Urban particulate matter (UPM) air pollution and vitamin D deficiency are detrimentally associated with respiratory health. This is hypothesized to be due in part to regulation of IL-17A, which UPM is reported to promote. Here, we used a myeloid dendritic cell (DC)-memory CD41 T cell co-culture system to characterize UPM-driven IL-17A 1 cells, investigate the mechanism by which UPM-primed DCs promote this phenotype, and address evidence for crossregulation by vitamin D. Clinical RelevanceUrban particulate matter air pollution and vitamin D deficiency are both detrimentally associated with airway function. This research describes an IL-23-dependent pathway by which urban particulate matter promotes a proinflammatory T helper 17 cell response, which is predicted to exacerbate respiratory diseases, and the capacity of vitamin D to oppose this effect. This supports the concept that restoring vitamin D sufficiency will help to counteract the detrimental properties of air pollution to maintain immune homeostasis.

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Section: Clinical Relevancementioning

confidence: 99%

Vitamin D Counteracts an IL-23–Dependent IL-17A⁺IFN-γ⁺ Response Driven by Urban Particulate Matter

Mann

Pfeffer

et al. 2017

Am J Respir Cell Mol Biol

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“…Our analyses indicate that serum 25(OH)D concentrations positively correlate with the densities of CD1a + dendritic cells and neutrophils at the tumor stroma but not with T cells that are considered more important in tumor immunosurveillance and have better-established prognostic value2122. The mechanism and the significance of the association we observed is not clear, but may be related to the well accepted immunoregulatory role of 25(OH)D on dendritic cells24 and requires further investigation. However, our findings do not suggest that tumor inflammatory infiltrate, in overall, is an important determinant of serum 25(OH)D levels in CRC patients or vice versa.…”

Section: Discussionmentioning

confidence: 68%

Decreased preoperative serum 25-Hydroxyvitamin D levels in colorectal cancer are associated with systemic inflammation and serrated morphology

Väyrynen

Mutt

Herzig

et al. 2016

Sci Rep

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Deficiency of vitamin D is associated with increased risk of several types of cancer including colorectal cancer (CRC). However, factors contributing to low levels of 25-hydroxyvitamin D [25(OH)D] in CRC are not clear. Therefore, in this study serum 25(OH)D levels in 117 CRC patients and 86 controls were analyzed and correlated with the clinicopathological data including morphological subtype (serrated or conventional), quantity of tumor infiltrating immune cells, levels of systemic inflammatory markers, and disease outcome. We found that the patients had lower serum 25(OH)D levels compared to the controls. Interestingly, among the patients mismatch repair deficiency, serrated morphology, and high body mass index associated with lowest serum 25(OH)D levels. In addition, patients operated in summer or autumn had higher serum 25(OH)D levels. Furthermore, serum 25(OH)D levels inversely correlated with several systemic inflammatory markers, e.g. serum C reactive protein, but did not associate with prognosis. Mechanism leading to vitamin D deficiency in these patients are not clear but could be related to the effects of systemic inflammation. Longitudinal studies are warranted to assess vitamin D deficiency as a potential risk factor for serrated colorectal polyps and adenocarcinoma.

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“…The immunomodulatory role of vitamin D is of increasing interest, and several in vitro studies have demonstrated downregulation of inflammation by vitamin D [246][247][248][249]. Moreover, hypovitaminosis D had been implicated in various inflammatory disorders including BD [250][251][252][253][254][255].…”

Section: Other Possible Markersmentioning

confidence: 99%

Etiology, Immunopathogenesis and Biomarkers in Behçet’s disease

Adeeb¹,

Khan²,

Stack³

et al. 2017

Behcet's Disease

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Behçet's disease (BD) is a type of vasculitis with many distinctive clinical manifestations and multifactorial immunopathogenesis. The cause of BD remains unknown, but it has been postulated that in a genetically predisposed or susceptible population, exogenous agents trigger the dysregulation of both autoinflammatory and autoimmune responses resulting in multisystem vasculitis. There are robust ongoing efforts across the globe to elucidate and identify signature markers to improve and assist in rapid diagnosis of the disease and to tailor the best therapy accordingly. While association of human leukocyte antigen (HLA)-B * 51 (B * 51:01 subtype) allele is well recognized as the strongest genetic susceptibility gene so far among genetically predisposed BD patients, further investigations using the latest technology have led to the identification of several novel single nucleotide polymorphisms (SNPs) and other associated genes involved in the pathogenesis. There are several "established" cytokines known to be involved in the pathogenesis of BD, which have been further implicated in the genome-wide association studies (GWAS)-based cytokine/receptor gene loci studies, as well as numerous "novel" cytokines, which are currently being studied and identified. This chapter offers insights into current knowledge and thoughts regarding the future of biomarkers in BD.

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Vitamin D immunoregulation through dendritic cells

Cited by 99 publications

References 81 publications

Vitamin D Counteracts an IL-23–Dependent IL-17A⁺IFN-γ⁺ Response Driven by Urban Particulate Matter

Vitamin D Counteracts an IL-23–Dependent IL-17A⁺IFN-γ⁺ Response Driven by Urban Particulate Matter

Decreased preoperative serum 25-Hydroxyvitamin D levels in colorectal cancer are associated with systemic inflammation and serrated morphology

Etiology, Immunopathogenesis and Biomarkers in Behçet’s disease

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Vitamin D immunoregulation through dendritic cells

Cited by 99 publications

References 81 publications

Vitamin D Counteracts an IL-23–Dependent IL-17A+IFN-γ+ Response Driven by Urban Particulate Matter

Vitamin D Counteracts an IL-23–Dependent IL-17A+IFN-γ+ Response Driven by Urban Particulate Matter

Decreased preoperative serum 25-Hydroxyvitamin D levels in colorectal cancer are associated with systemic inflammation and serrated morphology

Etiology, Immunopathogenesis and Biomarkers in Behçet’s disease

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Product

Resources

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Vitamin D Counteracts an IL-23–Dependent IL-17A⁺IFN-γ⁺ Response Driven by Urban Particulate Matter

Vitamin D Counteracts an IL-23–Dependent IL-17A⁺IFN-γ⁺ Response Driven by Urban Particulate Matter