The vitamin D receptor is required for iNKT cell development

Yu, Sanhong; Cantorna, Margherita T.

doi:10.1073/pnas.0711558105

Cited by 157 publications

(161 citation statements)

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“…Signaling from the iV14TCR is crucial for early iNKT cell development (7)(8)(9)(10). iNKT cell terminal maturation from stages 2 to 3 requires signal from the IL-15 and vitamin D receptors as well as the transcription factor T-bet and mediator subunit Med1 (11)(12)(13)(14). How T-bet is regulated for iNKT terminal maturation is poorly understood.…”

Section: Introductionmentioning

confidence: 99%

iNKT cells require TSC1 for terminal maturation and effector lineage fate decisions

Wu¹,

Yang²,

Yang³

et al. 2014

J. Clin. Invest.

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Section: Introductionmentioning

confidence: 99%

iNKT cells require TSC1 for terminal maturation and effector lineage fate decisions

Wu¹,

Yang²,

Yang³

et al. 2014

J. Clin. Invest.

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“…Vitamin D inhibits DC differentiation and maturation, their expression of major histocompatibility complex (MHC) class II, CD40, CD80, CD86 and IL-12 (whereas inducing the production of IL-10), leading to reduced T-cell stimulatory capacity [34][35][36]; it decreases the production of nitric oxide (NO), via downregulation of inducible nitric oxide synthase (iNOS) expression [37]. Moreover, it stimulates the development of natural killer T (NKT) cells, and it increases IL-4 and IFN-γ production by NKT cells [38]; it attenuates the proliferation of CD8+ T cells and their cytotoxic activity, by reducing the production of IL-2, IL-17 and IFN-γ; it exerts its immunomodulatory effects on T lymphocytes by inhibiting the production of pro-inflammatory Th1 cytokines (IL- is increased in demyelinating plaques [53][54][55], which may cause toxicity at later stages. Remyelination of demyelinated lesions has been observed in the early stages of MS [56][57][58], and it has been supported by neuroimaging findings [59][60][61][62][63][64][65].…”

Section: Vitamin D Deficiency and Multiple Sclerosis: Role In The Susmentioning

confidence: 99%

Vitamin D in Neurological Diseases: A Rationale for a Pathogenic Impact

Moretti

Morelli

Caruso

2018

Preprint

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It is widely known that vitamin D receptors have been found in neurons and glial cells and their highest expression is in the hippocampus, hypothalamus, thalamus and subcortical grey nuclei, and substantia nigra. The vitamin D helps the regulation of neurotrophin, neural differentiation and maturation, through the control operation of growing factors synthesis (ie NGF and GDNF), the trafficking of the septo-hyppocampal pathway, and the control of the synthesis process of different neuromodulators (such as Ach, DA, and GABA).Based on these assumptions, we have written this review in order to summarize the potential role of vitamin D in neurological pathologies. The work could be titanic, and might result very fuzzy and even incoherent, if we would not have conjectured to taper our first intentions and devoted our interests towards three mainstreams: demyelinating pathologies, vascular syndromes and neurodegeneration.Due to the lack of effective therapeutic options, a part from the disease modifying strategies, the role of different risk factors should be investigated in neurology, as far as their correction may lead to the improvement of the cerebral conditions.We have explored the relationships between the gene-environmental influence and long term vitamin D deficiency, as a risk factor for the development of different types of neurological disorders, along with the role and the rationale of therapeutic trials with vitamin D implementation. Peer-reviewed version available at Int. J. Mol. Sci. 2018, 19, 2245 doi:10.3390/ijms19082245 3 SEARCH STRATEGY AND SELECTION CRITERIAWe searched MEDLINE using the search terms: "vitamin D central nervous system" , both "vitamin D" and "central nervous system"; "vitamin D immune system/response", both "vitamin D" and "immune system" or "immune response"; "vitamin D multiple sclerosis risk", both "vitamin D" and "multiple sclerosis risk"; "vitamin D multiple sclerosis relapse", both "vitamin D" and "multiple sclerosis relapse"; "vitamin D multiple sclerosis magnetic resonance imaging", both "vitamin D" and "multiple sclerosis magnetic resonance imaging"; "vitamin D multiple sclerosis disability", both "vitamin D" and "multiple sclerosis disability"; "vitamin D supplementation/therapy/treatment multiple sclerosis", both "vitamin D supplementation" or "vitamin D therapy" or "vitamin D treatment" and "multiple sclerosis"; "vascular dementia", both as -vascular-and -dementia-, "subcortical vascular dementia", both assubcortical-and -dementia-, "Alzheimer's disease", "pathogenesis neurodegeneration" "amyloid", "cholinergic afferents", "arteriolosclerosis", "cerebral flow regulation", "stroke". Publications were selected mostly form the past 20years, but did not exclude frequently referenced and highly regarded older publications. . Congress abstracts and isolated case reports were not considered. We searched the reference lists of articles identified by this search strategy and selected those we judged relevant. Review articles and book chapters are cited to provide with ...

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“…For example, SLAM, SLAM-associated protein (SAP), and Src-family kinase FYN and NFB have been suggested to form a signaling pathway that controls iNKT cell development at a very early stage (2)(3)(4)(5)(6)(7)(8)(9)(10)(11). The cytokine IL-15, the vitamin D receptor, PTEN, SLP76 and transcription factors T-bet and AP-1 are all involved in the final maturation of iNKT cells (12)(13)(14)(15)(16)(17)(18).…”

Section: Cd8mentioning

confidence: 99%