干擾素(interferons)在50年前被發(fā)現(xiàn)，是人體對(duì)抗外來(lái)病菌的第一道防線,，當(dāng)病菌入侵,，細(xì)胞便開(kāi)始分泌干擾素，并將這個(gè)訊息分子傳遞,，開(kāi)始提醒所有細(xì)胞進(jìn)入警界狀態(tài),，這個(gè)訊息分子與發(fā)熱及發(fā)炎反應(yīng)有關(guān),。
迄今，已有三種主要的干擾素被發(fā)現(xiàn),，分別以希臘字母α, β及γ-interferon來(lái)命名,，其中α與β-interferon十分相似，甚至于會(huì)與細(xì)胞壁上相同的接受器(receptor)結(jié)合,，而γ-interferon就不同了,，它有自己專一的接受器，并且參與許多重要的免疫反應(yīng),，包括記住抗原(antigen presenting),，能讓免疫系統(tǒng)針對(duì)這些特定的抗原訂制對(duì)付它的抗體，或者活化免疫細(xì)胞以摧毀致病菌,。
魏茨曼科學(xué)院(Weizmann Institute)的研究人員發(fā)現(xiàn)γ-interferon并非獨(dú)自完成這些任務(wù),，Charles Dinarello教授的研究團(tuán)隊(duì)發(fā)現(xiàn)另一個(gè)在細(xì)胞內(nèi)的分子interleukin-1 alpha(IL-1α)，會(huì)與γ-interferon一起啟動(dòng)一連串的免疫反應(yīng),。此研究發(fā)表于近期的PNAS期刊,。
雖然γ-interferon及IL-1α這兩個(gè)分子是由兩個(gè)分別的系統(tǒng)所產(chǎn)生，但在免疫調(diào)節(jié)的反應(yīng)中都扮演相當(dāng)重要的角色,。Rubinstein教授說(shuō)：「IL-1α不會(huì)影響α或β-interferon,，但卻發(fā)現(xiàn)IL-1α與γ-interferon之間有協(xié)同作用，互相影響著對(duì)方,，能活化超過(guò)500個(gè)以上的基因,，當(dāng)然也包括那些帶來(lái)熱及肌肉疼痛的基因?！筊ubinstein教授說(shuō)：「由于啟動(dòng)γ-interferon抗病毒的活性需要耗費(fèi)很大的成本，這應(yīng)該是身體使用γ-interferon及IL-1α“dual key”系統(tǒng)的原因吧,！」
(資料來(lái)源 : Bio.com)
原始出處: http://www.bio.com/newsfeatures/newsfeatures_research.jhtml?cid=27500004
部分英文原文：
PNAS | March 20, 2007 | vol. 104 | no. 12 | 5044-5049
Antiviral and immunoregulatory activities of IFN- depend on constitutively expressed IL-1
Vladimir Hurgin*, Daniela Novick*, Ariel Werman*, Charles A. Dinarello, and Menachem Rubinstein*,
*Department of Molecular Genetics, The Weizmann Institute of Science, Rehovot 76100, Israel; and Department of Medicine, University of Colorado Health Sciences Center, Denver, CO 80262
Contributed by Charles A. Dinarello, December 28, 2006 (received for review October 24, 2006)
IFN- induces its immunoregulatory activities by activating genes mainly through the Jak-STAT signaling pathway. Here we show that what was considered to be intrinsic IFN- activities depend largely on the basal level of NF-B, which is maintained by constitutively expressed IL-1. The IL-1 receptor antagonist and antibodies to IL-1, but not to IL-1, inhibited the antiviral activity of IFN- by 90%, whereas no inhibition of type I IFN activity was observed. Similarly, the induction of many genes by IFN-, including HLA-DR, ICAM-1, IL-18BP, and genes mediating its antiviral activity, greatly depended on basal IL-1. Furthermore, IFN- induced serum IL-18 binding protein in wild-type mice but not in IL-1/ double-deficient mice. Thus, constitutively expressed IL-1 is critical for numerous IFN- activities.
Keywords：IFN regulatory factor-1 | NF-B | transcription regulation
