Epsilon Archive for Student Projects

Abstract

Rheumatoid arthritis is an autoimmune disorder in which our own immune system attacks our
own body tissues by mistake. It is a chronic inflammatory disease which primarily affects the
joints in the body. The damage is caused in the joints in the form of inflammations [1]. The main
parts affected by Rheumatoid arthritis are the peripheral joints which include finger joints,
wrists, toes and knees. Though this disease is prevalent for a long time the cause of the disease
is not known. It is believed that the genes present in the Major Histocompatibility Complex
region might contribute to the onset of rheumatoid arthritis in one way or another [2] [3] [4].
Various animal models are used to study the between rheumatoid arthritis and the genes in
Major Histocompatibility Complex. DA strains of rat are the widely used animal models for
rheumatology studies. In our laboratory it is observed that rats carrying MHC class III congenic
fragment, DA.1HR56 develop less severe diseases in our animal models of rheumatoid arthritis.
The animal models used in our lab are pristine‐induced arthritis (PIA) and oil‐induced arthritis
(OIA), both of which are T‐cell mediate disease models. Based on testing different subcongenic
fragments, we conclude that this protective phenotypes comes from a 220‐kb region in
chromosome 20 starting from 3649561 to 3864755; comprising approximately more than 20
genes like TNF, Lta, Ltb, Aif1, Bat2 and Lst1, a lot of which are potential candidate for immune
regulation. Some of these are much better investigated while some are not so well‐known.
Analyzing the 20 genes in the congenic region for polymorphism and its comparative gene
expression studies between DA strain and DA.1HR56 will help us to corner out the gene or
group of gene which leads to this protective phenotype. Based on these data, functional studies
of selected genes will be undertaken.