炎癥單核細(xì)胞是感染過程中,，病原體宿主的相互作用的早期關(guān)鍵反應(yīng)因素。
本研究發(fā)現(xiàn),，小鼠巨細(xì)胞病毒編碼的CC趨化因子,，MCK2，增強CCR2依賴的炎癥單核細(xì)胞招募,，以調(diào)節(jié)抗病毒的免疫力。
這一作用,，可抑制病毒特異性CD8 +T細(xì)胞擴(kuò)增和向效應(yīng)細(xì)胞毒性T淋巴細(xì)胞分化,，從而降低消除帶有病毒抗原細(xì)胞的能力和減緩病毒的清除,。將炎癥單核細(xì)胞過繼轉(zhuǎn)移到Ccr2/Ccl2雙基因敲除小鼠,，可降低對病毒的抗原特異性清除,。
因此,，巨細(xì)胞病毒增強天然CCR2依賴的免疫調(diào)節(jié)網(wǎng)絡(luò),，以通過產(chǎn)生一氧化氮,，調(diào)節(jié)適應(yīng)性免疫系統(tǒng)。這讓人想到主要在癌癥免疫調(diào)節(jié)中發(fā)揮作用的,，單核細(xì)胞亞型骨髓源性抑制細(xì)胞,。（生物谷bioon.com）
doi:10.1016/j.cell.2011.10.017
PMC:
PMID:
Cytomegalovirus Impairs Antiviral CD8+ T Cell Immunity by Recruiting Inflammatory Monocytes
Authors
Lisa P. Daley-Bauer, Grace M. Wynn, Edward S. Mocarski
Inflammatory monocytes are key early responders to infection that contribute to pathogen-host interactions in diverse ways. Here, we report that the murine cytomegalovirus-encoded CC chemokine, MCK2, enhanced CCR2-dependent recruitment of these cells to modulate antiviral immunity, impairing virus-specific CD8+ T cell expansion and differentiation into effector cytotoxic T lymphocytes, thus reducing the capacity to eliminate viral antigen-bearing cells and slowing viral clearance. Adoptive transfer of inflammatory monocytes into Ccr2/Ccl2/ mice impaired virus antigen-specific clearance. Cytomegalovirus therefore enhances a natural CCR2-dependent immune regulatory network to modulate adaptive immunity via nitric oxide production, reminiscent of the monocytic subtype of myeloid-derived suppressor cells primarily implicated in cancer immunomodulation.
