Dissection of the genetic complexity of arthritis using animal models.

Forskningsoutput: TidskriftsbidragÖversiktsartikel

Standard

Dissection of the genetic complexity of arthritis using animal models. / Holmdahl, Rikard.

I: Immunology Letters, Vol. 103, Nr. 2, 2006, s. 86-91.

Forskningsoutput: TidskriftsbidragÖversiktsartikel

Harvard

APA

CBE

MLA

Vancouver

Author

Holmdahl, Rikard. / Dissection of the genetic complexity of arthritis using animal models. I: Immunology Letters. 2006 ; Vol. 103, Nr. 2. s. 86-91.

RIS

TY - JOUR

T1 - Dissection of the genetic complexity of arthritis using animal models.

AU - Holmdahl, Rikard

N1 - The information about affiliations in this record was updated in December 2015. The record was previously connected to the following departments: Medical Inflammation Research (013212019)

PY - 2006

Y1 - 2006

N2 - Rheumatoid arthritis (RA) is a chronic inflammatory disease directed towards peripheral joints. As all common diseases it is associated with several genes and a multitude of environmental factors. In addition, in similarity with most other complex diseases, it is defined only on the basis of clinical signs and symptoms, it is therefore more properly classified as a syndrome rather than a distinct disease entity. This complexity of RA has led to difficulties in finding the underlying genes. In spite of large efforts it is still only the MHC class II region that reaches genome wide significance in confirmed studies. However, this has been known for decades and we are still unable to conclusively identify the underlying gene/s. We hypothesize that an MHC class II gene is involved and although we have detailed knowledge on both structure and function we do not know its possible pathogenic role in RA. In this review I will argue for the usefulness of animal models as a tool to identify genes and pathways associated with disease. The examples to be discussed are genes controlling the oxidative burst pathways and MHC class II genes.

AB - Rheumatoid arthritis (RA) is a chronic inflammatory disease directed towards peripheral joints. As all common diseases it is associated with several genes and a multitude of environmental factors. In addition, in similarity with most other complex diseases, it is defined only on the basis of clinical signs and symptoms, it is therefore more properly classified as a syndrome rather than a distinct disease entity. This complexity of RA has led to difficulties in finding the underlying genes. In spite of large efforts it is still only the MHC class II region that reaches genome wide significance in confirmed studies. However, this has been known for decades and we are still unable to conclusively identify the underlying gene/s. We hypothesize that an MHC class II gene is involved and although we have detailed knowledge on both structure and function we do not know its possible pathogenic role in RA. In this review I will argue for the usefulness of animal models as a tool to identify genes and pathways associated with disease. The examples to be discussed are genes controlling the oxidative burst pathways and MHC class II genes.

KW - MHC class II

KW - Animal models

KW - Genetics

KW - Arthritis

KW - Oxidative burst

U2 - 10.1016/j.imlet.2005.10.025

DO - 10.1016/j.imlet.2005.10.025

M3 - Review article

VL - 103

SP - 86

EP - 91

JO - Immunology Letters

T2 - Immunology Letters

JF - Immunology Letters

SN - 0165-2478

IS - 2

ER -