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Your search keyword '"Cytochrome P450 Family 7 metabolism"' showing total 3 results
Start Over Descriptor "Cytochrome P450 Family 7 metabolism" Topic receptors, g-protein-coupled
3 results on '"Cytochrome P450 Family 7 metabolism"'

1. Anti-microbial Functions of Group 3 Innate Lymphoid Cells in Gut-Associated Lymphoid Tissues Are Regulated by G-Protein-Coupled Receptor 183.

Author

Chu C, Moriyama S, Li Z, Zhou L, Flamar AL, Klose CSN, Moeller JB, Putzel GG, Withers DR, Sonnenberg GF, and Artis D

Subjects
Animals, Cell Movement, Citrobacter rodentium pathogenicity, Cytochrome P450 Family 7 metabolism, Enterobacteriaceae Infections pathology, Enterobacteriaceae Infections prevention & control, Enterobacteriaceae Infections veterinary, Humans, Hydroxycholesterols chemistry, Hydroxycholesterols metabolism, Immunity, Innate, Intestinal Mucosa cytology, Intestinal Mucosa metabolism, Ligands, Lymphoid Tissue cytology, Mice, Mice, Inbred C57BL, Mice, Knockout, Mucous Membrane cytology, Mucous Membrane metabolism, Receptors, G-Protein-Coupled antagonists & inhibitors, Receptors, G-Protein-Coupled genetics, Steroid Hydroxylases deficiency, Steroid Hydroxylases genetics, Steroid Hydroxylases metabolism, Lymphoid Tissue metabolism, Receptors, G-Protein-Coupled metabolism
Abstract

The intestinal tract is constantly exposed to various stimuli. Group 3 innate lymphoid cells (ILC3s) reside in lymphoid organs and in the intestinal tract and are required for immunity to enteric bacterial infection. However, the mechanisms that regulate the ILC3s in vivo remain incompletely defined. Here, we show that GPR183, a chemotactic receptor expressed on murine and human ILC3s, regulates ILC3 migration toward its ligand 7α,25-dihydroxycholesterol (7α,25-OHC) in vitro, and GPR183 deficiency in vivo leads to a disorganized distribution of ILC3s in mesenteric lymph nodes and decreased ILC3 accumulation in the intestine. GPR183 functions intrinsically in ILC3s, and GPR183-deficient mice are more susceptible to enteric bacterial infection. Together, these results reveal a role for the GPR183-7α,25-OHC pathway in regulating the accumulation, distribution, and anti-microbial and tissue-protective functions of ILC3s and define a critical role for this pathway in promoting innate immunity to enteric bacterial infection., (Copyright © 2018 The Authors. Published by Elsevier Inc. All rights reserved.)

Published
2018
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2. EBI2 Is Highly Expressed in Multiple Sclerosis Lesions and Promotes Early CNS Migration of Encephalitogenic CD4 T Cells.

Author

Wanke F, Moos S, Croxford AL, Heinen AP, Gräf S, Kalt B, Tischner D, Zhang J, Christen I, Bruttger J, Yogev N, Tang Y, Zayoud M, Israel N, Karram K, Reißig S, Lacher SM, Reichhold C, Mufazalov IA, Ben-Nun A, Kuhlmann T, Wettschureck N, Sailer AW, Rajewsky K, Casola S, Waisman A, and Kurschus FC

Subjects
Animals, Autoimmunity physiology, Central Nervous System physiology, Cytochrome P450 Family 7 metabolism, Disease Models, Animal, Encephalomyelitis, Autoimmune, Experimental pathology, Female, Interleukin-1beta metabolism, Interleukin-23 metabolism, Male, Mice, Mice, Inbred C57BL, Steroid Hydroxylases metabolism, Th17 Cells metabolism, Th17 Cells physiology, CD4-Positive T-Lymphocytes metabolism, CD4-Positive T-Lymphocytes physiology, Cell Movement physiology, Central Nervous System metabolism, Encephalomyelitis, Autoimmune, Experimental metabolism, Multiple Sclerosis metabolism, Receptors, G-Protein-Coupled metabolism
Abstract

Arrival of encephalitogenic T cells at inflammatory foci represents a critical step in development of experimental autoimmune encephalomyelitis (EAE), the animal model for multiple sclerosis. EBI2 and its ligand, 7α,25-OHC, direct immune cell localization in secondary lymphoid organs. CH25H and CYP7B1 hydroxylate cholesterol to 7α,25-OHC. During EAE, we found increased expression of CH25H by microglia and CYP7B1 by CNS-infiltrating immune cells elevating the ligand concentration in the CNS. Two critical pro-inflammatory cytokines, interleukin-23 (IL-23) and interleukin-1 beta (IL-1β), maintained expression of EBI2 in differentiating Th17 cells. In line with this, EBI2 enhanced early migration of encephalitogenic T cells into the CNS in a transfer EAE model. Nonetheless, EBI2 was dispensable in active EAE. Human Th17 cells do also express EBI2, and EBI2 expressing cells are abundant within multiple sclerosis (MS) white matter lesions. These findings implicate EBI2 as a mediator of CNS autoimmunity and describe mechanistically its contribution to the migration of autoreactive T cells into inflamed organs., (Copyright © 2017 The Author(s). Published by Elsevier Inc. All rights reserved.)

Published
2017
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3. The Role of the Oxysterol/EBI2 Pathway in the Immune and Central Nervous Systems.

Author

Rutkowska A, Dev KK, and Sailer AW

Subjects
Adaptive Immunity, Animals, Astrocytes metabolism, Cytochrome P450 Family 7 metabolism, Humans, Inflammation metabolism, Neurodegenerative Diseases metabolism, Receptors, G-Protein-Coupled genetics, Signal Transduction, Steroid Hydroxylases metabolism, Central Nervous System metabolism, Immune System metabolism, Oxysterols metabolism, Receptors, G-Protein-Coupled metabolism
Abstract

Oxysterols are pleiotropic messengers interacting with multiple receptor systems. One of the cognate receptors for oxysterols is EBI2, a G protein-coupled receptor highly expressed in the cells of the immune system. Here we discuss the receptor's role in the adapted immunity and inflammation as well as the receptor's expression and function in the CNS with the focus on astrocytes. We also discuss expression and signalling of oxysterol-producing enzymes such as CH25H and CYP7B1 in the CNS and the immune system. These steps will help to elucidate a possible role for this pathway in the physiology of the central and peripheral nervous system and its possible link to human disease.

Published
2016
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