英國(guó)一研究小組在最近一期出版的《免疫學(xué)雜志》上發(fā)表論文稱,，他們開(kāi)發(fā)出一種單克隆抗體，經(jīng)實(shí)驗(yàn)?zāi)Ｐ万?yàn)證,，該抗體與干擾素結(jié)合使用,，可有效對(duì)抗肺結(jié)核感染。研究人員認(rèn)為,，這一成果有助于科學(xué)家開(kāi)發(fā)出新的結(jié)核病治療手段,。
該研究小組由英國(guó)鄧迪大學(xué)、倫敦國(guó)王大學(xué)以及倫敦大學(xué)圣喬治學(xué)院的研究人員組成,。他們開(kāi)發(fā)的這種單克隆抗體是一種A類免疫球蛋白（lgA）,，屬于同質(zhì)性抗體，可識(shí)別結(jié)核桿菌,。它通過(guò)綁定結(jié)核桿菌細(xì)菌,，觸發(fā)人體免疫反應(yīng),，從而防止該細(xì)菌生長(zhǎng)蔓延。論文稱,，盡管單克隆抗體已被廣泛用于癌癥和炎癥性疾病的治療,，但這還是第一次研究表明，它可以用來(lái)治療結(jié)核病,。
免疫球蛋白是人體內(nèi)十分重要的免疫效應(yīng)分子,，因結(jié)構(gòu)不同可分為IgA、IgD,、IgE,、IgG和IgM五大類。研究人員認(rèn)為,，A類免疫球蛋白所具有的特性使其更易對(duì)抗結(jié)核病菌,。盡管實(shí)際臨床應(yīng)用之前還要進(jìn)行許多研究，但這一發(fā)現(xiàn)使科學(xué)家距離開(kāi)發(fā)出新的結(jié)核病治療方法更近了一步,。
肺結(jié)核是目前人類面臨的重大公共健康問(wèn)題之一,，全球每年有大約200萬(wàn)人死于該疾病，英國(guó)2010年的肺結(jié)核病例數(shù)則創(chuàng)下了10年來(lái)的新高,。雖然由于多種抗生素和預(yù)防藥物的產(chǎn)生使肺結(jié)核病例在世界范圍內(nèi)曾一度迅速減少,，但隨之而來(lái)，肺結(jié)核菌株的多重耐藥性也越來(lái)越明顯,，研制出新方法來(lái)預(yù)防和控制該種疾病顯得極為迫切,。（生物谷Bioon.com）
生物谷推薦原文出處：
The Journal of Immunology doi: 10.4049/jimmunol.1003189
A Novel Human IgA Monoclonal Antibody Protects against Tuberculosis
Sucharitha Balu*, Rajko Reljic?, Melanie J. Lewis?, Richard J. Pleass§?, Richard McIntosh?, Cees van Kooten‖, Marjolein van Egmond#, Stephen Challacombe*, Jenny M. Woof? and Juraj Ivanyi*
Abs have been shown to be protective in passive immunotherapy of tuberculous infection using mouse experimental models. In this study, we report on the properties of a novel human IgA1, constructed using a single-chain variable fragment clone (2E9), selected from an Ab phage library. The purified Ab monomer revealed high binding affinities for the mycobacterial α-crystallin Ag and for the human FcαRI (CD89) IgA receptor. Intranasal inoculations with 2E9IgA1 and recombinant mouse IFN-γ significantly inhibited pulmonary H37Rv infection in mice transgenic for human CD89 but not in CD89-negative littermate controls, suggesting that binding to CD89 was necessary for the IgA-imparted passive protection. 2E9IgA1 added to human whole-blood or monocyte cultures inhibited luciferase-tagged H37Rv infection although not for all tested blood donors. Inhibition by 2E9IgA1 was synergistic with human rIFN-γ in cultures of purified human monocytes but not in whole-blood cultures. The demonstration of the mandatory role of FcαRI (CD89) for human IgA-mediated protection is important for understanding of the mechanisms involved and also for translation of this approach toward development of passive immunotherapy of tuberculosis.
