Az 1-es típusú diabetes genetikája: Jelen és jövo

Translated title of the contribution: Genetics of type 1 diabetes: Present and future

Lukács Krisztina, P. Pánczél, N. Hosszúfalusi

Research output: Contribution to journalArticle

1 Citation (Scopus)

Abstract

Over the past decades the majority of genetic research focused on common diseases, and remarkable results were obtained for exploring the genetic background of type 1 diabetes. The classic linkage analyses and the modern genome-wide association studies demonstrated that the genetic background is the primary risk factor for beta-cell autoimmunity while the progression to clinical onset could be triggered by the genetic factors, epigenetic modifications of gene expression and environmental factors together. The new system biology concept can help to understand the mechanisms underlying the immune-mediated beta-cell destruction by generating networks based on data from whole genome scans, fine mapping and gene expression studies to develop targeted prevention and therapeutic strategies. In this paper, we discuss the present understanding of genetic factors which could initiate beta-cell autoimmunity (i.e. define the aetiology) and the genetic and epigenetic factors which might contribute to the progression to clinical disease in individuals with autoantibodies (i.e. define the pathogenesis).

Original languageHungarian
Pages (from-to)1731-1740
Number of pages10
JournalOrvosi Hetilap
Volume158
Issue number44
DOIs
Publication statusPublished - Nov 1 2017

Fingerprint

Type 1 Diabetes Mellitus
Autoimmunity
Epigenomics
Gene Expression
Genetic Research
Systems Biology
Genome-Wide Association Study
Autoantibodies
Genome
Genetic Background
Therapeutics

ASJC Scopus subject areas

  • Medicine(all)

Cite this

Az 1-es típusú diabetes genetikája : Jelen és jövo. / Krisztina, Lukács; Pánczél, P.; Hosszúfalusi, N.

In: Orvosi Hetilap, Vol. 158, No. 44, 01.11.2017, p. 1731-1740.

Research output: Contribution to journalArticle

@article{1e89135a30f14f14a596830910191ce3,
title = "Az 1-es t{\'i}pus{\'u} diabetes genetik{\'a}ja: Jelen {\'e}s j{\"o}vo",
abstract = "Over the past decades the majority of genetic research focused on common diseases, and remarkable results were obtained for exploring the genetic background of type 1 diabetes. The classic linkage analyses and the modern genome-wide association studies demonstrated that the genetic background is the primary risk factor for beta-cell autoimmunity while the progression to clinical onset could be triggered by the genetic factors, epigenetic modifications of gene expression and environmental factors together. The new system biology concept can help to understand the mechanisms underlying the immune-mediated beta-cell destruction by generating networks based on data from whole genome scans, fine mapping and gene expression studies to develop targeted prevention and therapeutic strategies. In this paper, we discuss the present understanding of genetic factors which could initiate beta-cell autoimmunity (i.e. define the aetiology) and the genetic and epigenetic factors which might contribute to the progression to clinical disease in individuals with autoantibodies (i.e. define the pathogenesis).",
keywords = "Epigenetics factors, Genetic background, Pathogenesis, System biology, Type 1 diabetes",
author = "Luk{\'a}cs Krisztina and P. P{\'a}ncz{\'e}l and N. Hossz{\'u}falusi",
year = "2017",
month = "11",
day = "1",
doi = "10.1556/650.2017.30903",
language = "Hungarian",
volume = "158",
pages = "1731--1740",
journal = "Orvosi Hetilap",
issn = "0030-6002",
publisher = "Akademiai Kiado",
number = "44",

}

TY - JOUR

T1 - Az 1-es típusú diabetes genetikája

T2 - Jelen és jövo

AU - Krisztina, Lukács

AU - Pánczél, P.

AU - Hosszúfalusi, N.

PY - 2017/11/1

Y1 - 2017/11/1

N2 - Over the past decades the majority of genetic research focused on common diseases, and remarkable results were obtained for exploring the genetic background of type 1 diabetes. The classic linkage analyses and the modern genome-wide association studies demonstrated that the genetic background is the primary risk factor for beta-cell autoimmunity while the progression to clinical onset could be triggered by the genetic factors, epigenetic modifications of gene expression and environmental factors together. The new system biology concept can help to understand the mechanisms underlying the immune-mediated beta-cell destruction by generating networks based on data from whole genome scans, fine mapping and gene expression studies to develop targeted prevention and therapeutic strategies. In this paper, we discuss the present understanding of genetic factors which could initiate beta-cell autoimmunity (i.e. define the aetiology) and the genetic and epigenetic factors which might contribute to the progression to clinical disease in individuals with autoantibodies (i.e. define the pathogenesis).

AB - Over the past decades the majority of genetic research focused on common diseases, and remarkable results were obtained for exploring the genetic background of type 1 diabetes. The classic linkage analyses and the modern genome-wide association studies demonstrated that the genetic background is the primary risk factor for beta-cell autoimmunity while the progression to clinical onset could be triggered by the genetic factors, epigenetic modifications of gene expression and environmental factors together. The new system biology concept can help to understand the mechanisms underlying the immune-mediated beta-cell destruction by generating networks based on data from whole genome scans, fine mapping and gene expression studies to develop targeted prevention and therapeutic strategies. In this paper, we discuss the present understanding of genetic factors which could initiate beta-cell autoimmunity (i.e. define the aetiology) and the genetic and epigenetic factors which might contribute to the progression to clinical disease in individuals with autoantibodies (i.e. define the pathogenesis).

KW - Epigenetics factors

KW - Genetic background

KW - Pathogenesis

KW - System biology

KW - Type 1 diabetes

UR - http://www.scopus.com/inward/record.url?scp=85032625846&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=85032625846&partnerID=8YFLogxK

U2 - 10.1556/650.2017.30903

DO - 10.1556/650.2017.30903

M3 - Article

C2 - 29086595

AN - SCOPUS:85032625846

VL - 158

SP - 1731

EP - 1740

JO - Orvosi Hetilap

JF - Orvosi Hetilap

SN - 0030-6002

IS - 44

ER -