Suppression of NK cells and regulatory T lymphocytes in cats naturally infected with feline infectious peritonitis virus.

Suppression of NK cells and regulatory T lymphocytes in cats naturally infected with feline infectious peritonitis virus.
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DOI:
10.1016/j.vetmic.2013.01.042
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发表时间:
2013-05-31
影响因子:
3.3
通讯作者:
Nauwynck HJ
Nauwynck HJ
中科院分区:
农林科学2区
文献类型:
--
作者:
Vermeulen BL;Devriendt B;Olyslaegers DA;Dedeurwaerder A;Desmarets LM;Favoreel HW;Dewerchin HL;Nauwynck HJ

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在这项研究中,强烈的细胞介导的免疫力(CMI)是必不可少的,可以防止猫科动物感染性腹膜炎病毒(FIPV)。在量化的FIPV感染期间,对先天和自适应CMI的中心参与者进行了检查。与健康的非感染对照动物相比,FIP猫的肾脏没有任何差异。 FIP猫中血液来源的NK细胞的植物型分析显示,激活标记(CD16和CD25)和迁移标记(CD11b和CD62L)的上调,而LN衍生的NK细胞仅表现出仅来自CD16和CD62L的NK细胞上调。与健康的猫相比,FIPV感染的猫的细胞毒性也明显较小。 )。针对NK细胞和Treg的疗法在FIPV感染过程中增强其数量和/或功能。
A strong cell-mediated immunity (CMI) is thought to be indispensable for protection against infection with feline infectious peritonitis virus (FIPV) in cats. In this study, the role of natural killer (NK) cells and regulatory T cells (Tregs), central players in the innate and adaptive CMI respectively, was examined during natural FIPV infection. When quantified, both NK cells and Tregs were drastically depleted from the peripheral blood, mesenteric lymph node (LN) and spleen in FIP cats. In contrast, mesentery and kidney from FIP cats did not show any difference when compared to healthy non-infected control animals. In addition, other regulatory lymphocytes (CD4+CD25−Foxp3+ and CD3+CD8+Foxp3+) were found to be depleted from blood and LN as well. Phenotypic analysis of blood-derived NK cells in FIP cats revealed an upregulation of activation markers (CD16 and CD25) and migration markers (CD11b and CD62L) while LN-derived NK cells showed upregulation of only CD16 and CD62L. LN-derived NK cells from FIPV-infected cats were also significantly less cytotoxic when compared with healthy cats. This study reveals for the first time that FIPV infection is associated with severe suppression of NK cells and Tregs, which is reflected by cell depletion and lowered cell functionality (only NK cells). This will un-doubtfully lead to a reduced capacity of the innate immune system (NK cells) to battle FIPV infection and a decreased capacity (Tregs) to suppress the immunopathology typical for FIP. However, these results will also open possibilities for new therapies targeting specifically NK cells and Tregs to enhance their numbers and/or functionality during FIPV infection.
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