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Characterization of cytokine/chemokine networks promoting localized recruitment of immune effector cells for antiviral defense.

機(jī)譯：細(xì)胞因子/趨化因子網(wǎng)絡(luò)的表征，可促進(jìn)免疫效應(yīng)細(xì)胞的局部募集以用于抗病毒防御。

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Effective delivery of innate and adaptive immune mechanisms depends on the recruitment of effector cells to sites of infection. Our laboratory has identified a cytokine and chemokine cascade that is induced upon infection with MCMV and plays a critical role in inflammation and the balance between life and death. It has been shown that IFN-alpha/beta-mediated effects promote the production of MIP-1alpha by mediating the recruitment of MIP-1alpha-producing macrophages to liver during MCMV infection. This results in NK cell inflammation and delivery of localized IFN-gamma in order to support antiviral defense at this site. However, it remains to be determined if IFN-alpha/beta induces an intermediary chemokine directly required for macrophage recruitment. Herein, I demonstrate that IFN-alpha/beta effects promote MCP-1 expression by resident liver cells. Additionally, I show that MCP-1/CCR2 interactions are required for recruitment of macrophages, NK cells and promotion of MIP-1alpha and IFN-gamma expression in liver, leading to viral clearance and survival. I also investigated mechanisms promoting IFN-alpha/beta production in liver during MCMV. Here, I demonstrate that plasmacytoid dendritic cells are major contributors to IFN-alpha/beta production and that IFN-alpha/beta expression and hepatic viral clearance is dependent upon the presence of MyD88 but not TLR9. Finally, we investigated the requirements for T cell recruitment to liver following infection. At time points corresponding with T cell accumulation, we observed protein expression of both Mig and IP-10, two potent T cell chemoattractants. Neutralization of these chemokines as well as studies using CXCR3-deficient animals, revealed a function for these chemokines in mediating T cell recruitment and promoting antiviral defense. In addition, CCR2 was also identified as a key player in directing T cell trafficking to liver, but these effects were not mediated by MCP-1. Taken together, these studies contribute to our understanding of in vivo chemokine biology and function by defining cytokine and chemokine networks and the mechanisms promoting their expression. Collectively, these effects are required for effective antiviral defense in tissues.
機(jī)譯：先天性和適應(yīng)性免疫機(jī)制的有效傳遞取決于效應(yīng)細(xì)胞募集到感染部位。我們的實(shí)驗(yàn)室已經(jīng)確定了MCMV感染后誘導(dǎo)的細(xì)胞因子和趨化因子級(jí)聯(lián)反應(yīng)，并且在炎癥以及生與死之間的平衡中起關(guān)鍵作用。已經(jīng)表明，IFN-α/β介導(dǎo)的作用通過在MCMV感染期間介導(dǎo)將產(chǎn)生MIP-1α的巨噬細(xì)胞募集到肝臟而促進(jìn)了MIP-1α的產(chǎn)生。這會(huì)導(dǎo)致NK細(xì)胞發(fā)炎并傳遞局部IFN-γ，以支持該部位的抗病毒防御。但是，是否確定IFN-α/β是否誘導(dǎo)巨噬細(xì)胞募集直接需要的中間趨化因子仍有待確定。在本文中，我證明了IFN-α/β效應(yīng)可促進(jìn)駐留肝細(xì)胞表達(dá)MCP-1。此外，我表明，MCP-1 / CCR2相互作用對(duì)于募集巨噬細(xì)胞，NK細(xì)胞以及促進(jìn)肝臟中MIP-1alpha和IFN-γ的表達(dá)是必需的，從而導(dǎo)致病毒清除和存活。我還研究了在MCMV期間促進(jìn)肝臟中IFN-α/β產(chǎn)生的機(jī)制。在這里，我證明漿細(xì)胞樣樹突狀細(xì)胞是產(chǎn)生IFN-α/β的主要因素，并且IFN-α/β的表達(dá)和肝病毒清除率取決于MyD88的存在，而不取決于TLR9。最后，我們調(diào)查了感染后T細(xì)胞募集至肝臟的要求。在與T細(xì)胞積累相對(duì)應(yīng)的時(shí)間點(diǎn)，我們觀察到了兩種有效的T細(xì)胞趨化因子Mig和IP-10的蛋白表達(dá)。這些趨化因子的中和以及使用CXCR3缺陷動(dòng)物的研究表明，這些趨化因子在介導(dǎo)T細(xì)胞募集和促進(jìn)抗病毒防御方面具有功能。此外，CCR2也被認(rèn)為是指導(dǎo)T細(xì)胞向肝臟運(yùn)輸?shù)年P(guān)鍵因素，但這些作用并非由MCP-1介導(dǎo)?？傊?，這些研究通過定義細(xì)胞因子和趨化因子網(wǎng)絡(luò)以及促進(jìn)其表達(dá)的機(jī)制，有助于我們對(duì)體內(nèi)趨化因子生物學(xué)和功能的理解。總的來說，這些作用是有效的組織抗病毒防御所必需的。

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