Genetics of Behçet's disease

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Genetics of Behçet's disease. / Morton, Laura T; Situnayake, Deva; Wallace, Graham R.

In: Current Opinion in Rheumatology, Vol. 28, No. 1, 01.2016, p. 39-44.

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Morton, Laura T ; Situnayake, Deva ; Wallace, Graham R. / Genetics of Behçet's disease. In: Current Opinion in Rheumatology. 2016 ; Vol. 28, No. 1. pp. 39-44.

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@article{21d257d132784579a863e0246336d2ec,
title = "Genetics of Beh{\c c}et's disease",
abstract = "PURPOSE OF REVIEW: This article discusses recent genetic and epigenetic associations involved in the pathogenesis of Beh{\c c}et's disease.RECENT FINDINGS: Genetic studies have supported the strong association of human leukocyte antigen-B and Beh{\c c}et's disease, and high production of tumour necrosis factor and low production of interleukin (IL)-10, which have led to therapy based on controlling these effects. Polymorphisms that affect the response to pathogens (TLR and FUT2) are leading to increased interest in responses to microbiomes. Inflammation in Beh{\c c}et's disease results in vascular damage and several single nucleotide polymorphisms in chemokine and adhesion molecules may be involved in this process. Increased levels of inflammatory cytokines including IL-1β and IL-17 have been linked to altered expression of microRNAs, miR155, miR21 and miR23b. DNA methylation changes in monocytes and lymphocytes have been described that affect the function of these cells.SUMMARY: Genetic and epigenetic changes affecting cells and molecules involved in Beh{\c c}et's disease offer new pathways for research, including cytoskeletal protein function, that will provide new targets for therapy, and potentially address the ethnic differences seen in validation of gene studies.",
author = "Morton, {Laura T} and Deva Situnayake and Wallace, {Graham R}",
year = "2016",
month = jan,
doi = "10.1097/BOR.0000000000000234",
language = "English",
volume = "28",
pages = "39--44",
journal = "Current Opinion in Rheumatology",
issn = "1040-8711",
publisher = "Lippincott Williams and Wilkins",
number = "1",

}

RIS

TY - JOUR

T1 - Genetics of Behçet's disease

AU - Morton, Laura T

AU - Situnayake, Deva

AU - Wallace, Graham R

PY - 2016/1

Y1 - 2016/1

N2 - PURPOSE OF REVIEW: This article discusses recent genetic and epigenetic associations involved in the pathogenesis of Behçet's disease.RECENT FINDINGS: Genetic studies have supported the strong association of human leukocyte antigen-B and Behçet's disease, and high production of tumour necrosis factor and low production of interleukin (IL)-10, which have led to therapy based on controlling these effects. Polymorphisms that affect the response to pathogens (TLR and FUT2) are leading to increased interest in responses to microbiomes. Inflammation in Behçet's disease results in vascular damage and several single nucleotide polymorphisms in chemokine and adhesion molecules may be involved in this process. Increased levels of inflammatory cytokines including IL-1β and IL-17 have been linked to altered expression of microRNAs, miR155, miR21 and miR23b. DNA methylation changes in monocytes and lymphocytes have been described that affect the function of these cells.SUMMARY: Genetic and epigenetic changes affecting cells and molecules involved in Behçet's disease offer new pathways for research, including cytoskeletal protein function, that will provide new targets for therapy, and potentially address the ethnic differences seen in validation of gene studies.

AB - PURPOSE OF REVIEW: This article discusses recent genetic and epigenetic associations involved in the pathogenesis of Behçet's disease.RECENT FINDINGS: Genetic studies have supported the strong association of human leukocyte antigen-B and Behçet's disease, and high production of tumour necrosis factor and low production of interleukin (IL)-10, which have led to therapy based on controlling these effects. Polymorphisms that affect the response to pathogens (TLR and FUT2) are leading to increased interest in responses to microbiomes. Inflammation in Behçet's disease results in vascular damage and several single nucleotide polymorphisms in chemokine and adhesion molecules may be involved in this process. Increased levels of inflammatory cytokines including IL-1β and IL-17 have been linked to altered expression of microRNAs, miR155, miR21 and miR23b. DNA methylation changes in monocytes and lymphocytes have been described that affect the function of these cells.SUMMARY: Genetic and epigenetic changes affecting cells and molecules involved in Behçet's disease offer new pathways for research, including cytoskeletal protein function, that will provide new targets for therapy, and potentially address the ethnic differences seen in validation of gene studies.

U2 - 10.1097/BOR.0000000000000234

DO - 10.1097/BOR.0000000000000234

M3 - Article

C2 - 26599381

VL - 28

SP - 39

EP - 44

JO - Current Opinion in Rheumatology

JF - Current Opinion in Rheumatology

SN - 1040-8711

IS - 1

ER -