CD24: missing gene reduces MS risk
Posted: Tue Apr 17, 2007 10:06 am
Below is the author's summary of a report into a genetic mutation which appears to help protect against MS and Lupus. The mutation occurs at a point which should make the protein CD 24, but two base pairs are missing so the body produces less.
CD24 plays an important part in the immune system, and reducing the amount of it cuts not only the risk of getting MS or lupus in the first place, but also the severity and progression of MS if you do get it. Of course, we all know that there is a huge question mark over the whole autoimmunity thing, but until its proved or disproved, I'll take any piece of research going!
"When an individual's immune system attacks self tissues or organs, he/she develops autoimmune diseases. Although it is well established that multiple genes control susceptibility to autoimmune diseases, most of the genes remain unidentified. In addition, although different autoimmune diseases have a common immunological basis, a very small number of genes have been identified that affect multiple autoimmune diseases. Here we show that a variation in CD24 is a likely genetic factor for the risk and progression of two types of autoimmune diseases, including multiple sclerosis (MS), an organ-specific autoimmune disease affecting the central nervous system, and systemic lupus erythematosus, a systemic autoimmune disease. Our data indicated that if an individual's CD24 gene has a specific two-nucleotide deletion in the noncoding region of CD24 mRNA, his/her risk of developing MS or SLE is reduced by 2- to 3-fold. As a group, MS patients with the two-nucleotide deletion will likely have a slower disease progression. Biochemical analysis indicated that the deletion leads to rapid decay of CD24 mRNA, which should result in reduced synthesis of the CD24 protein. Our data may be useful for the treatment and diagnosis of autoimmune diseases"
Authors:Wang1,2, Shili Lin3, Kottil W. Rammohan4, Zhenqiu Liu3, Jin-qing Liu5, Run-hua Liu1,2, Nikki Guinther5, Judy Lima4, Qunmin Zhou6, Tony Wang5, Xincheng Zheng6, Dan J. Birmingham7, Brad H. Rovin7, Lee A. Hebert7, Yeeling Wu8, D. Joanne Lynn4, Glenn Cooke7, C. Yung Yu8, Pan Zheng1,2, Yang Liu1,2*
The entire article is available free of charge on PloS at:
http://genetics.plosjournals.org/perlse ... 9#toclink1
But to be honest the author's summary is about all I could understand!
CD24 plays an important part in the immune system, and reducing the amount of it cuts not only the risk of getting MS or lupus in the first place, but also the severity and progression of MS if you do get it. Of course, we all know that there is a huge question mark over the whole autoimmunity thing, but until its proved or disproved, I'll take any piece of research going!
"When an individual's immune system attacks self tissues or organs, he/she develops autoimmune diseases. Although it is well established that multiple genes control susceptibility to autoimmune diseases, most of the genes remain unidentified. In addition, although different autoimmune diseases have a common immunological basis, a very small number of genes have been identified that affect multiple autoimmune diseases. Here we show that a variation in CD24 is a likely genetic factor for the risk and progression of two types of autoimmune diseases, including multiple sclerosis (MS), an organ-specific autoimmune disease affecting the central nervous system, and systemic lupus erythematosus, a systemic autoimmune disease. Our data indicated that if an individual's CD24 gene has a specific two-nucleotide deletion in the noncoding region of CD24 mRNA, his/her risk of developing MS or SLE is reduced by 2- to 3-fold. As a group, MS patients with the two-nucleotide deletion will likely have a slower disease progression. Biochemical analysis indicated that the deletion leads to rapid decay of CD24 mRNA, which should result in reduced synthesis of the CD24 protein. Our data may be useful for the treatment and diagnosis of autoimmune diseases"
Authors:Wang1,2, Shili Lin3, Kottil W. Rammohan4, Zhenqiu Liu3, Jin-qing Liu5, Run-hua Liu1,2, Nikki Guinther5, Judy Lima4, Qunmin Zhou6, Tony Wang5, Xincheng Zheng6, Dan J. Birmingham7, Brad H. Rovin7, Lee A. Hebert7, Yeeling Wu8, D. Joanne Lynn4, Glenn Cooke7, C. Yung Yu8, Pan Zheng1,2, Yang Liu1,2*
The entire article is available free of charge on PloS at:
http://genetics.plosjournals.org/perlse ... 9#toclink1
But to be honest the author's summary is about all I could understand!