炎症单核细胞是感染过程中，病原体宿主的相互作用的早期关键反应因素。
本研究发现，小鼠巨细胞病毒编码的CC趋化因子，MCK2，增强CCR2依赖的炎症单核细胞招募，以调节抗病毒的免疫力。
这一作用，可抑制病毒特异性CD8 +T细胞扩增和向效应细胞毒性T淋巴细胞分化，从而降低消除带有病毒抗原细胞的能力和减缓病毒的清除。将炎症单核细胞过继转移到Ccr2/Ccl2双基因敲除小鼠，可降低对病毒的抗原特异性清除。
因此，巨细胞病毒增强天然CCR2依赖的免疫调节网络，以通过产生一氧化氮，调节适应性免疫系统。这让人想到主要在癌症免疫调节中发挥作用的，单核细胞亚型骨髓源性抑制细胞。（生物谷bioon.com）
doi:10.1016/j.cell.2011.10.017
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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.
