AsianScientist (Feb. 4, 2016) – In an international study, researchers have found ten new gene regions in Asian populations that confer increased susceptibility to lupus, an autoimmune disease.
Systemic lupus erythematosus (SLE), commonly referred to as lupus, is a chronic disease where the body’s immune system becomes overactive and attacks its own organs, such as skin, muscle, blood, heart and kidneys.
Its name originates from the characteristic butterfly-shaped rash patients sometimes display on their faces, which resembles the bite of a wolf, or lupus in Latin. No cure is available and treatments focus on disease management.
“Development of SLE is strongly affected by genetic components. It has been known that genetic variations accounts for 66 percent of risk for SLE,” Kim Kwangwoo of Hanyang University for Rheumatic Diseases in Korea, a co-first author of the study, told Asian Scientist Magazine.
Despite knowing that there is a strong genetic component, identifying the genes involved in SLE has been challenging as SLE is controlled by multiple genes. Currently known genes can only explain for the disease in about ten percent of patients.
In the present study, published in Nature Genetics, researchers from Korea, China, Japan, Malaysia and the United States recruited more than 4,000 patients and 12,000 healthy controls, comprising of Koreans, Chinese and Japanese.
Since there is a higher incidence of SLE in Asians than Europeans, the current study looked at genetic differences or variants between Asian SLE patients and healthy controls.
By focusing on only the immune-related genes instead of the whole genome, the researchers identified ten new variants that conferred increased SLE susceptibility. These variants participate in a variety of functions, including signaling, turning different genes on and even maintaining the stability of chromosomes.
As the cause of SLE is unclear, the genes identified in this study can help bring researchers one step closer to understanding the mechanism of disease as well as serve as potential drug targets.
“Our short-term goal is to understand the biological mechanism where the identified SLE-risk alleles confer risk for SLE,” said Kim.
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