日本筑波大学免疫学教授涩谷彰在6日的《自然·免疫学》杂志网络版上发表文章说，他率领的研究小组发现了能够抑制花粉症、哮喘以及特应性皮炎等过敏反应的分子。涩谷彰指出：“如果能够开发出加强这一分子活动的药物，将有望彻底根治过敏症。”
涩谷彰说，花粉和蜱等致敏原侵入人体后，与某种抗体结成一体，而一旦与肥大细胞结合，肥大细胞就会释放出可引起炎症的化学物质，从而使机体出现过敏症状。他认为，具有特定氨基酸排列的分子应该能够遏制肥大细胞的活性化。根据这一思路，研究人员在人体肥大细胞的细胞膜上找到了这种分子，激活这种分子后，从肥大细胞释放出的化学物质减少了大约一半。
随后，研究人员通过基因操作制造出不含有这种分子的试验鼠，结果发现，与其他实验老鼠相比，这种试验鼠在接触致敏原后更易出现过敏反应。
涩谷彰说，在过敏症发病机制方面，老鼠和人基本相同，他希望这一发现有助于开发出治疗过敏的新药。(生物谷Bioon.com)
生物谷推荐原文出处：
Nature Immunology doi:10.1038/ni.1886
An immunoglobulin-like receptor, Allergin-1, inhibits immunoglobulin E–mediated immediate hypersensitivity reactions
Kaori Hitomi,Satoko Tahara-Hanaoka,Satoru Someya,Akira Fujiki,Hideaki Tada,Tetsuya Sugiyama,Shiro Shibayama,Kazuko Shibuya& Akira Shibuya
Anaphylaxis is a life-threatening immediate hypersensitivity reaction triggered by antigen capture by immunoglobulin E (IgE) bound to the high-affinity IgE receptor (FcεRI) on mast cells. However, the regulatory mechanism of mast cell activation is not completely understood. Here we identify an immunoglobulin-like receptor, Allergin-1, that contains an immunoreceptor tyrosine-based inhibitory motif (ITIM)-like domain, and show it was preferentially expressed on mast cells. Mouse Allergin-1 recruited the tyrosine phosphatases SHP-1 and SHP-2 and the inositol phosphatase SHIP. Coligation of Allergin-1 and FcεRI suppressed IgE-mediated degranulation of bone marrow–derived cultured mast cells. Moreover, mice deficient in Allergin-1 developed enhanced passive systemic and cutaneous anaphylaxis. Thus, Allergin-1 suppresses IgE-mediated, mast cell–dependent anaphylaxis in mice.
