生物谷报道：结核分枝菌是一种能引发肺结核的细菌，世界上有1/3的人口被这种细菌所感染，基本上每1秒种就有一个新感染案例，从而造成全球性的健康问题。如今，研究人员在6月号的《自然—免疫学》期刊上报告说，他们发现结核分枝菌分泌出的一种蛋白质能够严重抑制早期的免疫反应。
以前的研究发现，结核分枝细菌分泌的ESAT-6蛋白质与免疫系统对结核分枝细菌的无效反应有关，如今，Joyoti Basu和同事评估了这种蛋白质的功能。Toll样受体(TLRs)是机体通过感知病原微生物体并激活细胞直接产生免疫防御的天然免疫受体，Basu等发现，纯化的ESAT-6能阻断特定的免疫受体蛋白质——Toll样受体的信号，产生这种机制的关键是ESAT-6与一种Toll受体——TLR2在巨噬细胞表面上的特定相互作用，巨噬细胞是一种重要的免疫前哨。他们发现，通过与TLR2的结合，ESAT-6诱导出一种关闭所有Toll样受体功能的信号。
研究人员指出，阻断ESAT-6与TLR2间的相互作用也许是一种治疗肺结核的潜在方法，而模拟ESAT-6与TLR2间的相互作用将有助于抑制过度的炎症反应。
Figure 1 - ESAT-6 inhibits LPS-driven production of IL-12p40.
(a) ELISA of IL-12p40 in the supernatants of RAW cells treated with LPS (1 g/ml) alone or with CFP-10 (C; 5 g/ml) or ESAT-6–CFP-10 complex (E–C; 5 g/ml) or varying concentrations (horizontal axes) of recombinant ESAT-6 protein purified from E. coli. (b) ELISA of IL-12p40 in supernatants of RAW cells treated with LPS and 0, 1 or 3 g/ml of recombinant ESAT-6 protein purified from HEK293 cells. (c,d) ELISA of IL-6 (c) or TNF (d) in supernatants of RAW cells treated with LPS, recombinant ESAT-6 protein purified from E. coli, or both. Data are the mean + s.d. of three experiments.
原文出处：
Nature Immunology June 2007, Volume 8 No 6
Direct extracellular interaction between the early secreted antigen ESAT-6 of Mycobacterium tuberculosis and TLR2 inhibits TLR signaling in macrophages - pp610 - 618
Sushil Kumar Pathak, Sanchita Basu, Kunal Kumar Basu, Anirban Banerjee, Shresh Pathak, Asima Bhattacharyya, Tsuneyasu Kaisho, Manikuntala Kundu & Joyoti Basu
doi:10.1038/ni1468
相关基因：
TLR2
Official Symbol TLR2 and Name: toll-like receptor 2 [Homo sapiens]
Other Aliases: CD282, TIL4
Other Designations: toll/interleukin 1 receptor-like 4
Chromosome: 4; Location: 4q32
Annotation: Chromosome 4, NC_000004.10 (154824890..154846692)
MIM: 603028
GeneID: 7097
