Reticuloendotheliosis Virus Inhibits the Immune Response Acting on Lymphocytes from Peripheral Blood of Chicken.
Reticuloendotheliosis Virus Inhibits the Immune Response Acting on Lymphocytes from Peripheral Blood of Chicken.
复制标题
网状内皮病病毒抑制了作用于鸡外周血的淋巴细胞上的免疫反应。
DOI：
10.3389/fphys.2018.00004
复制
发表时间：
2018
影响因子：
4
通讯作者：
Chen G
中科院分区：
文献类型：
--
作者：
Bi Y;Xu L;Qiu L;Wang S;Liu X;Zhang Y;Chen Y;Zhang Y;Xu Q;Chang G;Chen G
鸡网状内皮组织增生病病毒（REV）可引起免疫器官萎缩和免疫抑制。REV的致病机制知之甚少。本研究的目的是利用RNA测序技术分析REV对鸡外周血淋巴细胞免疫功能和细胞增殖的影响。总的来说，2977差异表达基因（DEG）之间的细胞感染REV或没有检查，56 DEG相关的细胞增殖和130 DEG相关的免疫被确定。MTT、Q-PCR和FCM结果表明，REV通过FOXO和p53途径抑制S/G1期细胞的转化，从而减少淋巴细胞的数量。类似地，REV感染会通过MAPK-AP 1经由Toll样受体-、NOD样受体-和Salmonella感染途径破坏淋巴细胞的免疫防御，从而减少IL 8和IL 18的分泌。此外，淋巴细胞的减少也可能是导致IL 8和IL 18水平降低的原因，并且淋巴细胞的拯救仍然通过FOXO和p53途径被激活。此外，淋巴细胞对REV的免疫应答将通过Toll样受体/NOD样受体/沙门氏菌-MAPK-AP 1途径上调NOD 1、MYD 88和AP 1的表达而激活。提示REV可通过抑制淋巴细胞增殖和免疫系统而影响外周血淋巴细胞。NOD 1、MYD 88和AP 1是通过Toll样受体/NOD-like受体/沙门氏菌-MAPK-AP 1途径激活免疫应答的关键基因。这些发现为揭示鸡REV感染的分子机制奠定了基础，并提供了新的线索。
Chicken reticuloendotheliosis virus (REV) causes the atrophy of immune organs and immuno-suppression. The pathogenic mechanisms of REV are poorly understood. The aim of this study was to use RNA sequencing to analyse the effect of REV on immunity and cell proliferation in chicken lymphocytes from peripheral blood in vitro. Overall, 2977 differentially expressed genes (DEGs) were examined from cells between infected with REV or no; 56 DEGs related to cell proliferation and 130 DEGs related to immunity were identified. MTT, Q-PCR, and FCM indicated that REV reduced the number of lymphocytes by inhibiting the transition of S/G1 phase through FOXO and p53 pathways. Similarly, REV infection would destroy the immune defense of lymphocytes through MAPK-AP1 via Toll-like receptor-, NOD-like receptor-, and salmonella infection pathways to reduce the secretion of IL8 and IL18. In addition, the reduction of lymphocytes also might be responsible for the lower levels of IL8 and IL18, and the rescue of lymphocytes would been activated still through FOXO and p53 pathways. Moreover, the immune response for REV in lymphocytes would activate by up-regulating the expression of NOD1, MYD88, and AP1 through Toll-like receptor-/NOD-like receptor/salmonella-MAPK-AP1 pathways. These results indicate that REV could affect lymphocytes from peripheral blood by inhibit the cell proliferation and the immune system. It also was revealed that NOD1, MYD88, and AP1 were the key genes to activate the immune response through Toll-like receptor-/NOD-like receptor/salmonella-MAPK-AP1 pathways. These findings establish the groundwork and provide new clues for deciphering the molecular mechanism underlying REV infection in chickens.
登录
查看更多内容
与肺淋巴骨料相关的IL-18在严重COPD中驱动IFNγ产生。
影响因子：
5.8
作者：
Briend E;Ferguson GJ;Mori M;Damera G;Stephenson K;Karp NA;Sethi S;Ward CK;Sleeman MA;Erjefält JS;Finch DK
通讯作者：
Finch DK
影响因子：
1.4
作者：
Gibbs, PS;Maurer, JJ;Wooley, RE
通讯作者：
Wooley, RE
DOI：
10.1186/s13058-014-0482-y
发表时间：
2014-12-09
期刊：
Breast cancer research : BCR
影响因子：
--
作者：
Hill R;Kalathur RK;Callejas S;Colaço L;Brandão R;Serelde B;Cebriá A;Blanco-Aparicio C;Pastor J;Futschik M;Dopazo A;Link W
通讯作者：
Link W
影响因子：
3.1
作者：
Buchholz, Kerry R.;Stephens, Richard S.
通讯作者：
Stephens, Richard S.
影响因子：
1.2
作者：
Cheng, Ziqiang;Shi, Youfei;Cui, Zhizhong
通讯作者：
Cui, Zhizhong