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[Niacin deficiency and cutaneous immunity].

Abstract
Niacin, also known as vitamin B3, is required for the synthesis of coenzymes, nicotinamide adenine dinucleotide (NAD) and nicotinamide adenine dinucleotide phosphate (NADP). Niacin binds with G protein-coupled receptor (GPR) 109A on cutaneous Langerhans cells and causes vasodilation with flushing in head and neck area. Niacin deficiency due to excessive alcohol consumption, certain drugs or inadequate uptake in diet causes pellagra, a photosensitivity dermatitis. Recently several studies have revealed the mechanism of photosensitivity in niacin deficiency, which may pave a way for new therapeutic approaches. The expression level of prostaglandin E synthase (PTGES) is up-regulated in the skin of both pellagra patients and niacin deficient pellagra mouse models. In addition, pellagra is mediated through prostaglandin E₂-EP4 (PGE₂-EP4) signaling via reactive oxygen species (ROS) production in keratinocytes. In this article, we have reviewed the role of niacin in immunity and the mechanism of niacin deficiency-induced photosensitivity.
AuthorsAtsuko Ikenouchi-Sugita, Kazunari Sugita
JournalNihon Rinsho Men'eki Gakkai kaishi = Japanese journal of clinical immunology (Nihon Rinsho Meneki Gakkai Kaishi) Vol. 38 Issue 1 Pg. 37-44 ( 2015) ISSN: 1349-7413 [Electronic] Japan
PMID25765687 (Publication Type: Journal Article, Review)
Chemical References
  • Reactive Oxygen Species
  • Receptors, G-Protein-Coupled
  • Receptors, Prostaglandin E, EP4 Subtype
  • Niacin
  • Intramolecular Oxidoreductases
  • PTGES protein, human
  • Prostaglandin-E Synthases
  • Ptges protein, mouse
  • Dinoprostone
Topics
  • Animals
  • Dinoprostone
  • Humans
  • Intramolecular Oxidoreductases (metabolism)
  • Keratinocytes (metabolism)
  • Langerhans Cells (metabolism)
  • Mice
  • Niacin (deficiency, metabolism, physiology)
  • Pellagra (etiology, metabolism)
  • Prostaglandin-E Synthases
  • Reactive Oxygen Species
  • Receptors, G-Protein-Coupled (metabolism)
  • Receptors, Prostaglandin E, EP4 Subtype
  • Signal Transduction
  • Skin (immunology, metabolism)
  • Up-Regulation
  • Vasodilation

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