波士顿大学牙科学院研究者研制出炎症降低的小鼠模型，结果发表在昨天的《美国国立科学院院报》杂志上。
波士顿大学的研究者发现，LITAF转录因子（脂多糖LPS诱导的α-肿瘤坏死因子）通过与已知的途径和以前研究的NF-kB转录调控途径完全不同的途径来控制炎症。
通过已知的NF-kB 途径如Remicade，Embrel, and Humira 调控的α-肿瘤坏死因子药物占据了很大的市场。LITAF转录因子为炎症紊乱及其他的免疫状况的治疗提供了新的方法。研究者出售这种体内模型，以便发现治疗关节炎和节段性回肠炎等炎症紊乱疾病的药物。
在研究中，波士顿大学研究者培育出缺失编码LITAF蛋白基因的小鼠。他们发现，比较试验中LITAF阳性对照小鼠来说，LITAF缺失小鼠以较低的水平诱导一些细胞活素类。缺失LITAF小鼠对LPS诱导的致死率有更大的耐药性。
“巨噬细胞特异的缺失LITAF动物的发生为估价LITAF在炎症中的功能，为更多炎症疾病寻找抗-LITAF药物开辟了新的良机。”波士顿大学Salomon Amar博士评价。LITAF转录因子是Amar于1999年发现的。
申请此项专利的研究者正在探索其他的分子与LITAF是否存在着协同增效作用。
英文原文：
In a paper published yesterday in The Proceedings of the National Academy of Science (PNAS), researchers from Boston University School of Dental Medicine generated a mouse model exhibiting reduced inflammation.
The Boston University researchers found that the transcription factor LITAF (Lipopolysaccharide [LPS]-Induced TNF-Alpha Factor) controls inflammation through a completely different pathway than the better known and studied NF-kB transcriptional regulator.
Drugs regulating TNF-alpha through the better-known NF-kB pathway such as Remicade, Embrel, and Humira represent a multibillion market. The LITAF transcription factor offers a new approach to treating inflammatory disorders along with other immunological conditions. Researchers are offering this in vivo model for sale to spearhead discovery of drugs against inflammatory disorders such as arthritis and Crohn's disease.
In the study, Boston University researchers created a mouse lacking the gene that encodes for the LITAF protein. They found that several cytokines were induced at lower levels in the LITAF-deficient mice compared with the levels observed in the LITAF-positive control mice. Specifically, the deficient mice were more resistant to LPS-induced lethality.
"The generation of the macrophage-specific LITAF-deficient animals opens new opportunities for assessing the role of LITAF in inflammation in hopes of designing anti-LITAF drugs for major inflammatory diseases," says Dr. Salomon Amar of Boston University, the lead author of the paper. Amar discovered the LITAF transcription factor in 1999.
Researchers, who have applied to patent the mouse, are now working on whether other molecules work in synergy with LITAF.
