Vitamin D, a neuro-immunomodulator: Implications for neurodegenerative and autoimmune diseases

• Published in: Psychoneuroendocrinology Vol. 34; pp. S265 - S277
• Main Authors: Fernandes de Abreu, D.A, Eyles, D, Féron, F
• Format: Journal Article
• Language: English
• Published: England Elsevier Ltd 01.12.2009; Elsevier
• Subjects: Animals; Autoimmune Diseases - metabolism; Central Nervous System Diseases - metabolism; Endocrinology & Metabolism; Humans; Immune system; Life Sciences; Mental Disorders - metabolism; Models, Biological; Models, Immunological; Multiple sclerosis; Nervous system; Neurodegenerative Diseases - metabolism; Neuroimmunomodulation - physiology; Neurons and Cognition; Neurotransmitter Agents - immunology; Neurotransmitter Agents - physiology; Psychiatry; Steroid hormone; Vitamin D; Vitamin D - physiology; Nervous system; Multiple sclerosis; Vitamin D; Steroid hormone; Immune system
• ISSN: 0306-4530; 1873-3360
• DOI: 10.1016/j.psyneuen.2009.05.023

Summary It has been known for more than 20 years that vitamin D exerts marked effects on immune and neural cells. These non-classical actions of vitamin D have recently gained a renewed attention since it has been shown that diminished levels of vitamin D induce immune-mediated symptoms in animal models of autoimmune diseases and is a risk factor for various brain diseases. For example, it has been demonstrated that vitamin D (i) modulates the production of several neurotrophins, (ii) up-regulates Interleukin-4 and (iii) inhibits the differentiation and survival of dendritic cells, resulting in impaired allo-reactive T cell activation. Not surprisingly, vitamin D has been found to be a strong candidate risk-modifying factor for Multiple Sclerosis (MS), the most prevalent neurological and inflammatory disease in the young adult population. Vitamin D is a seco-steroid hormone, produced photochemically in the animal epidermis. The action of ultraviolet light (UVB) on 7-dehydrocholesterol results in the production of pre-vitamin D which, after thermo-conversion and two separate hydroxylations, gives rise to the active 1,25-dihydroxyvitamin D. Vitamin D acts through two types of receptors: (i) the vitamin D receptor (VDR), a member of the steroid/thyroid hormone superfamily of transcription factors, and (ii) the MARRS (membrane associated, rapid response steroid binding) receptor, also known as Erp57/Grp58. In this article, we review some of the mechanisms that may underlie the role of vitamin D in various brain diseases. We then assess how vitamin D imbalance may lay the foundation for a range of adult disorders, including brain pathologies (Parkinson's disease, epilepsy, depression) and immune-mediated disorders (rheumatoid arthritis, type I diabetes mellitus, systemic lupus erythematosus or inflammatory bowel diseases). Multidisciplinary scientific collaborations are now required to fully appreciate the complex role of vitamin D in mammal metabolism.