谁知道为什么这个病这么难治的？

阿浩

谁知道为什么这个病这么难治的？

李志强博士

和免疫有关的自身免疫病没有一个是好治的，白癜风亦然。

scncnbzp

<font face="Verdana" color="#da2549"><strong>李志强博士,你认为BB与自身的</strong><font color="#000000">免疫功能有关吗,那是不是要查一下免疫功能是否正常,但是免疫又分细胞免疫和体液免疫,具体应该查哪些方面?</font></font>

peterwu1025

因为就目前医学水平还没有攻克它，再就是它的发病机制很不明确，所以它是很不好治的！

不想流泪

拭目以待 我们有的是时间去等待

李志强博士

<p>免疫是非常复杂的，现在还远远没有认识清除。现在临床上能进行的免疫检查项目是非常肤浅的，BB患者如果做这些检查一般不会有明显的问题。可以参考下列文章：</p><p></p><p>揭开自身免疫疾病黑箱之谜<br/><a href="http://www.eurekalert.org/pub_releases/2007-01/wifb-cot011607.php">http://www.eurekalert.org/pub_releases/2007-01/wifb-cot011607.php</a></p><p>ublic release date: 21-Jan-2007<br/>Cracking open the black box of autoimmune disease</p><p>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. <br/>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。<br/>"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."<br/>Whitehead成员和美国麻省理工学院生物学教授Richard Young，是将要发表在1月21刊《自然》上的文章的第一作者，他说：这个研究可能缩短自身免疫疾病新的治疗方法产生的进程，因为这组基因，现在我们能够寻找更加精确的合理的治疗方法。<br/>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. <br/>免疫系统经常被描绘成象军队，一个防御网络能够保护机体免于被入侵。从这点看，一组称为T细胞的血细胞处在免疫防线的第一线，防止病原体入侵。<br/>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. <br/>这些T细胞受到第二组称为调节T细胞的细胞管理。调节T细胞防止生物学上的“友军火力误伤”以确保T细胞不攻击身体自身组织。调节T细胞障碍不能控制第一线活力导致自身免疫疾病。<br/>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. <br/>科学家们先前受到它们自己的称为Foxp3的主(导)基因调节因子控制。主基因调节因子约束特定的基因并控制它们的活性水平，依次影响细胞行为。实际上，当Foxp3停止作用，机体就不能再产生调节T细胞。一旦发生这种情况，第一线的T细胞就损伤多个器官并导致I型糖尿病症状和Crohn's病。然而，直到现在科学家们还没有了解Foxp3是如何控制调节T细胞的，因为他们对于Foxp3控制下的真实基因一点都不知道。</p><p>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. <br/>在Richard Young's Whitehead实验室的研究人员和Dana-Farber癌症研究所的免疫学家Harald von Boehme一起紧密合作，运用DNA微点阵技扫描整个基因组显示并定位了Foxp3所控制的基因。大致有30个基因发现受到Foxp3的直接调控并且有个名为Ptpn22的基因特别表示出强烈的亲和力。<br/>"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."<br/>“这个关系是引人注目的，因为Ptpn22与I型糖尿病类风湿性关节炎狼疮Graves'病有很强的相关性，但是这个基因以前没有被与调节T细胞的功能联系起来。”文章的第一作者Young实验室的Alexander Marson说道“发现这种联系对我们来说是个重大的时刻。它证实我们正走在鉴别自身免疫相关基因的正确道路上。”<br/>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. <br/>研究者们还没有准确知道Foxp3是如何使调节T细胞避免自身免疫的。但是这一组Foxp3的靶基因提供了这些细胞的初始路线图，这对于了解它们如何控制一个正常的免疫反应是重要的。<br/>"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."<br/>Young说“自身免疫疾病确实对人类的健康的带来巨大伤害，但严格从分子水平说，自身免疫是一个黑箱，当我们发现导致这些疾病的分子机制，我们能够从对症治疗转移到发展这些疾病自身的治疗方法。” <br/></p>

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