Department of Microbiology, Immunology Programme, National University of Singapore, Singapore, Singapore.
PLoS One. 2011;6(11):e27849. doi: 10.1371/journal.pone.0027849. Epub 2011 Nov 18.
Foxp3⁺CD4⁺ regulatory T cells represent a T cell subset with well-characterized immunosuppressive effects during immune homeostasis and chronic infections, and there is emerging evidence to suggest these cells temper pulmonary inflammation in response to acute viral infection. Recent studies have demonstrated treatment with PC61 CD25-depleting antibody potentiates inflammation in a murine model of RSV infection, while paradoxically delaying recruitment of CD8⁺ T cells to the site of inflammation. The present study therefore sought to examine the role of these cells in a murine model of acute influenza A virus infection through the administration of PC61 CD25-depleting antibody. PC61 antibody is able to partially deplete CD25⁺Foxp3⁺ regulatory T cells to a comparable degree as seen within previous work examining RSV, however this does not alter influenza A-virus induced mortality, weight loss, viral clearance and cellularity within the lung. Collectively, these data demonstrate that partial depletion of CD4⁺CD25⁺ regulatory T cells with PC61 antibody does not alter the course of influenza A virus infection.
Foxp3⁺CD4⁺调节性 T 细胞是一种具有特征性免疫抑制作用的 T 细胞亚群，在免疫稳态和慢性感染中发挥作用，有新的证据表明这些细胞可以调节急性病毒感染引起的肺部炎症。最近的研究表明，用 PC61 CD25 耗竭抗体治疗可增强 RSV 感染的小鼠模型中的炎症，而矛盾的是，这会延迟 CD8⁺T 细胞向炎症部位的募集。因此，本研究通过给予 PC61 CD25 耗竭抗体，在急性甲型流感病毒感染的小鼠模型中研究这些细胞的作用。PC61 抗体能够部分耗尽 CD25⁺Foxp3⁺调节性 T 细胞，其程度与之前研究 RSV 时所见相似，但这并不改变甲型流感病毒感染引起的死亡率、体重减轻、病毒清除和肺部细胞数量。综上所述，这些数据表明，用 PC61 抗体部分耗尽 CD4⁺CD25⁺调节性 T 细胞不会改变甲型流感病毒感染的过程。
