A particular genetic region that has been increasingly recognized as the strongest genetic link to psoriasis apparently has an even more vital role in the chronic skin disease than it was thought to be. This result comes in the light of a new study from the University of Utah.
The experts claim that the presence of HLA-Cw*0602, a gene variation or allele on chromosome 6 is apparently found to be connected with psoriasis by several investigators. Supposedly it is a ‘major genetic determinant’ of psoriasis but other close by genetic variations also seem to take part in an independent role in contributing to the disease.
Gerald G. Krueger, M.D., professor of dermatology, Benning Presidential Endowed Chair holder, and a co-author on the study commented “The HLA-Cw*0602 gene variation stands alone as a high risk for psoriasis. A major question has been: are there other genetic variations in this region that associate with psoriasis?”
Apparently the study has identified two other genetic variations on chromosome 6 that also have an important alliance with psoriasis. People who have all three genetic variations are supposedly almost nine times more at a threat for psoriasis.
Psoriasis is a chronic, non-contagious autoimmune disease that affects the skin and joints and causes red, scaly patches to appear on the skin. Approximately 7.5 million people in the United States are affected by psoriasis. A painful inflammation of the joints known as psoriatic arthritis apparently affects about 25 percent of the subjects.
University study experts, led by first author Bing-Jian Feng, Ph.D., postdoctoral fellow, and senior author David E. Goldgar, Ph.D., professor of dermatology in the University Of Utah School Of Medicine analyzed the data in partnership with colleagues from the University of Michigan and Washington University.
To find out those who had the strongest association with psoriasis, a previous study known as Nature genetics applied novel technology to look into nearly 500,000 genetic variants (single nucleotide polymorphisms or ANPs) in 1,359 people with psoriasis and 1,400 without psoriasis. The experts extended the study to include 5,048 people with psoriasis and 5,051 without the disease after supposedly identifying 18 SNPs with the highest connection to psoriasis. From that, they recognized four new genetic ‘hotspots’ for psoriasis and apparently established two others that Krueger and colleagues had identified in earlier studies.
Data from the Nature genetics study was also used. Two statistical techniques i.e. imputation and logistic regression analysis, to apparently determine those genes with a much higher extent of precision that has the chief relationship with psoriasis were employed by Feng, Goldgar and their colleagues. Using imputation, they were supposedly able to predict the *0602 status of all subjects in the latest Nature genetics study. By this, they seem to have achieved two things. First, it raised the assurance that *0602 is apparently the key genetic variation on this chromosome. Second, it seemed to allow them to determine if there was any other linked genetic variation in this area.
Identification of two other loci (fixed position on a chromosome) that are independently linked with psoriasis (MICA/HLA-B and c6orf10) are apparently resulted by removing the strong effect of *0602. The threat for the disease was supposedly increased by these two loci. Feng and Goldgar report that when all three genetic variations are present, the possibility of psoriasis is apparently 8.9 times higher than when none of these are present. Experts observed an independent patient population in China, which seemed to substantiate their conclusions.
Kruegar is of the opinion that even though *0602 and the linked but independent genetic variations accounted apparently have a chief genetic contribution to psoriasis, several other genes supposedly also play a role. In the past 2 years, the number of DNA sites found to have strong associations with psoriasis seem to have doubled.
It is published in the issue of PLoS Genetics.