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【medical-news】揭开自身免疫疾病黑箱之谜
Public release date: 21-Jan-2007
Cracking open the black box of autoimmune disease
CAMBRIDGE, Mass. (January 21, 2007) -- Autoimmune diseases such as type 1 diabetes, lupus and rheumatoid arthritis occur when the immune system fails to regulate itself. But researchers have not known precisely where the molecular breakdowns responsible for such failures occur. Now, a team of scientists from the Whitehead Institute and the Dana-Farber Cancer Institute have identified a key set of genes that lie at the core of autoimmune disease, findings that may help scientists develop new methods for manipulating immune system activity.
"This may shorten the path to new therapies for autoimmune disease," says Whitehead Member and MIT professor of biology Richard Young, senior author on the paper that will appear January 21 online in Nature. "With this new list of genes, we can now look for possible therapies with far greater precision."
The immune system is often described as a kind of military unit, a defense network that guards the body from invaders. Seen in this way, a group of white blood cells called T cells are the frontline soldiers of immune defense, engaging invading pathogens head on.
These T cells are commanded by a second group of cells called regulatory T cells. Regulatory T cells prevent biological "friendly fire" by ensuring that the T cells do not attack the body's own tissues. Failure of the regulatory T cells to control the frontline fighters leads to autoimmune disease.
Scientists previously discovered that regulatory T cells are themselves controlled by a master gene regulator called Foxp3. Master gene regulators bind to specific genes and control their level of activity, which in turn affects the behavior of cells. In fact, when Foxp3 stops functioning, the body can no longer produce working regulatory T cells. When this happens, the frontline T cells damage multiple organs and cause symptoms of type 1 diabetes and Crohn's disease. However, until now, scientists have barely understood how Foxp3 controls regulatory T cells because they knew almost nothing about the actual genes under Foxp3's purview.
Researchers in Richard Young's Whitehead lab, working closely with immunologist Harald von Boehmer of the Dana-Farber Cancer Institute, used a DNA microarray technology developed by Young to scan the entire genome of T cells and locate the genes controlled by Foxp3. There were roughly 30 genes found to be directly controlled by Foxp3 and one, called Ptpn22, showed a particularly strong affinity.
"This relation was striking because Ptpn22 is strongly associated with type 1 diabetes, rheumatoid arthritis, lupus and Graves' disease, but the gene had not been previously linked to regulatory T-cell function," says Alexander Marson, a MD/PhD student in the Young lab and lead author on the paper. "Discovering this correlation was a big moment for us. It verified that we were on the right track for identifying autoimmune related genes."
The researchers still don't know exactly how Foxp3 enables regulatory T cells to prevent autoimmunity. But the list of the genes that Foxp3 targets provides an initial map of the circuitry of these cells, which is important for understanding how they control a healthy immune response.
"Autoimmune diseases take a tremendous toll on human health, but on a strictly molecular level, autoimmunity is a black box," says Young. "When we discover the molecular mechanisms that drive these conditions, we can migrate from treating symptoms to developing treatments for the disease itself." 本人已认领该文编译，48小时后若未提交译文，请其他战友自由认领。 揭开自身免疫疾病黑箱之谜
http://www.eurekalert.org/pub_releases/2007-01/wifb-cot011607.php
Public release date: 21-Jan-2007
07-1-21公开发表
Cracking open the black box of autoimmune disease
CAMBRIDGE, Mass. (January 21, 2007) -- Autoimmune diseases such as type 1 diabetes, lupus and rheumatoid arthritis occur when the immune system fails to regulate itself. But researchers have not known precisely where the molecular breakdowns responsible for such failures occur. Now, a team of scientists from the Whitehead Institute and the Dana-Farber Cancer Institute have identified a key set of genes that lie at the core of autoimmune disease, findings that may help scientists develop new methods for manipulating immune system activity.
美国剑桥麻省07-1-21消息----自身免疫性疾病例如I型糖尿病、狼疮和类风湿性关节炎经常发生在免疫系统不能自我调节的时候。但研究人员还没有明确知道与这些疾病发生相关的分子故障在哪里。现在来自美国麻省Whitehea研究所和Dana-Farber癌症研究所的一组科学家鉴定了一组关键基因，它们是自身免疫性疾病的关键所在。这个发现可能帮助科学家们发展一种新的方法处理免疫系统活性。
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作者:admin@医学,生命科学 2011-08-29 17:12
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