自然杀伤细胞在人3型副流感病毒感染期间调节T细胞增殖。
Natural killer cells regulate T-cell proliferation during human parainfluenza virus type 3 infection.
作者信息
Noone Cariosa M, Paget Elaine, Lewis Ellen A, Loetscher Marius R, Newman Robert W, Johnson Patricia A
机构信息
Viral Immunology laboratory, School of Biotechnology, Dublin City University, Glasnevin, Dublin 9, Ireland.
出版信息
J Virol. 2008 Sep;82(18):9299-302. doi: 10.1128/JVI.00717-08. Epub 2008 Jul 9.
Abstract
Human parainfluenza virus type 3 (HPIV3) is a major respiratory pathogen in humans. Failure to induce immunological memory associated with HPIV3 infection has been attributed to inhibition of lymphocyte proliferation. We demonstrate that the inability of mixed lymphocytes to respond to virally infected antigen-presenting cells is due to an interleukin-2-dependent, nonapoptotic mechanism involving natural killer (NK) cells and their influence is exerted in a contact-dependent manner. These results suggest a novel regulatory mechanism for NK cells during HPIV3 infection, offering an explanation for viral persistence and poor memory responses.
摘要
人副流感病毒3型（HPIV3）是人类主要的呼吸道病原体。与HPIV3感染相关的免疫记忆未能诱导，这归因于淋巴细胞增殖的抑制。我们证明，混合淋巴细胞对病毒感染的抗原呈递细胞无反应的能力，是由于一种依赖白细胞介素-2的非凋亡机制，该机制涉及自然杀伤（NK）细胞，并且它们的影响以接触依赖的方式发挥作用。这些结果提示了HPIV3感染期间NK细胞的一种新型调节机制，为病毒持续存在和记忆反应不佳提供了解释。
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