Multiple Sclerosis helped by UV – possibly via cytokines, etc.
Ultraviolet radiation, vitamin D and multiple sclerosis.
Neurodegener Dis Manag. 2015 Oct;5(5):413-24. doi: 10.2217/nmt.15.33. Epub 2015 Oct 19.
Lucas RM 1,2, Byrne SN 3, Correale J 4, Ilschner S 5, Hart PH2.
1National Centre for Epidemiology & Population Health, Research School of Population Health, The Australian National University, Canberra, Australia.
2Telethon Kids Institute, University of Western Australia, Perth, Western Australia, Australia.
3Sydney Medical School, University of Sydney, Sydney, Australia.
4Department of Neurology, Raul Carrea Institute for Neurological Research, FLENI, Buenos Aires, Argentina.
5Independent researcher.
The items in both categories MS and UV are listed here:
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The items in both categories MS and Inflammation are listed here:
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There is compelling epidemiological evidence that the risk of developing multiple sclerosis is increased in association with low levels of sun exposure, possibly because this is associated with low vitamin D status. Recent work highlights both vitamin D and non-vitamin D effects on cellular immunity that suggests that higher levels of sun exposure and/or vitamin D status are beneficial for both MS risk and in ameliorating disease progression.
Here we review this recent evidence, focusing on regulatory cells, dendritic cells, and chemokines and cytokines released from the skin following exposure to ultraviolet radiation.
KEYWORDS: B regulatory cells; cis-urocanic acid; dendritic cells; multiple sclerosis; ultraviolet radiation; vitamin D
PMID: 26477548 DOI: 10.2217/nmt.15.33
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Table 2. Uv-regulated cytokines and their possible role in multiple sclerosis. | |||
|
Cytokine |
Uv-induced trigger |
Main cutaneous source |
Possible role in MS |
|
Upregulated | |||
|
IL-10 |
DNAdamage |
Epithelial cells |
Anti-inflammatory |
|
Vitamin D |
Dendritic cells |
Lowers TNF | |
|
Mast cells |
Increases T„ [117] | ||
|
IL-1P |
ATP? Caspase? [118] |
Macrophages |
Proinflammatory |
|
Keratinocytes |
Increases permeability of the blood-brain barrier [119] | ||
|
IL-6 |
DNA damage |
Keratinocytes [120] |
Proinflammatory |
|
T-cells Macrophages Fibroblasts |
Increases Th17 [121] | ||
|
IL-8 |
UV-B |
Fibroblasts [122] |
Reduced by IFN-P treatment [123] |
|
Topical 1,25(OH)D inhibits release [124] |
Keratinocytes Mast cells | ||
|
GM-CSF |
DNA damage |
T cells Macrophages Keratinocytes [126] |
Associated with relapses [125] |
|
TNF |
IL-1 |
Macrophages Mast cells T cells Keratinocytes [127] |
Proinflammatory |
|
IL-33 |
Platelet activating factor |
Fibroblasts [114] |
Paradoxically elevated in MS patients [128] |
|
Keratinocytes [114] |
Attenuates EAE by suppressing IL-17 and IFN [129] | ||
|
Downregulated | |||
|
IFN-y |
Cytokine signaling molecules 1 and 3 [130] |
Keratinocytes |
Macrophage/microglia stimulation |
|
Il-17/23 |
Transcriptional modulation, IL-6 [118] |
Th 17 cells |
Expressed in brain lesions of MS patients; induces expression of inflammatory genes in astrocytes [131] |
|
Keratinocytes | |||
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DC: Dendritic cell; MS: Multiple sclerosis. | |||