一項(xiàng)最新研究發(fā)現(xiàn),，有些人很容易感染腦膜炎,，但有些人對(duì)腦膜炎天生免疫，這是因?yàn)樗麄兊幕虼嬖诓煌?。這項(xiàng)發(fā)現(xiàn)有助于研制針對(duì)B型腦膜炎球菌的疫苗,。
英國(guó)帝國(guó)理工學(xué)院等機(jī)構(gòu)研究人員在新一期《自然·遺傳學(xué)》（Nature Genetics）雜志上報(bào)告說，他們和同行收集了英國(guó),、荷蘭,、奧地利和西班牙等國(guó)約1500名腦膜炎患者的基因數(shù)據(jù)，并將其與另外5000多名健康人的基因進(jìn)行了對(duì)比,。結(jié)果發(fā)現(xiàn),，在與一種名為H因子的蛋白相關(guān)基因中，易患腦膜炎人群與健康人存在差異,。
研究人員發(fā)現(xiàn),，H因子本身在人體免疫系統(tǒng)中幫助辨別和殺死入侵細(xì)菌，但在易患腦膜炎人群中,，腦膜炎球菌卻可以“劫持”H因子,，像“特洛伊木馬”那樣利用它來騙過人體免疫系統(tǒng)，從而使人們感染腦膜炎,。
研究人員指出,，這項(xiàng)研究有助于研制針對(duì)B型腦膜炎球菌的疫苗。目前,，不少類型的腦膜炎現(xiàn)在已有針對(duì)性的疫苗,，但不包括由B型腦膜炎球菌引起的腦膜炎。（生物谷Bioon.com）
生物谷推薦原文出處：
Nature Genetics doi:10.1038/ng.640
Genome-wide association study identifies variants in the CFH region associated with host susceptibility to meningococcal disease
Sonia Davila1,15, Victoria J Wright2,15, Chiea Chuen Khor1, Kar Seng Sim3, Alexander Binder4, Willemijn B Breunis5, David Inwald2, Simon Nadel2, Helen Betts2, Enitan D Carrol6, Ronald de Groot7, Peter W M Hermans7, Jan Hazelzet8, Marieke Emonts8,9, Chui Chin Lim1, Taco W Kuijpers5, Federico Martinon-Torres10,11, Antonio Salas12,13, Werner Zenz4, Michael Levin2,15 & Martin L Hibberd1,15 for the International Meningococcal Genetics Consortium14
Meningococcal disease is an infection caused by Neisseria meningitidis. Genetic factors contribute to host susceptibility and progression to disease, but the genes responsible for disease development are largely unknown1, 2, 3. We report here a genome-wide association study for host susceptibility to meningococcal disease using 475 individuals with meningococcal disease (cases) and 4,703 population controls from the UK. We performed, in Western European and South European cohorts (consisting of 968 cases and 1,376 controls), two replication studies for the most significant SNPs. A cluster of complement factor SNPs replicated independently in both cohorts, including SNPs within complement factor H (CFH) (rs1065489 (p.936D<E), P = 2.2 × 10?11) and in CFH-related protein 3 (CFHR3)(rs426736, P = 4.6 × 10?13). N. meningitidis is known to evade complement-mediated killing by the binding of host CFH to the meningococcal factor H–binding protein (fHbp)4. Our study suggests that host genetic variation in these regulators of complement activation plays a role in determining the occurrence of invasive disease versus asymptomatic colonization by this pathogen.
