The Interaction between JAK-STAT Signalling and Immune Regulation in Grouper

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基本資料

Project title

Code/計畫編號

MOST103-2313-B019-012-MY3

Translated Name/計畫中文名

石斑魚JAK-STAT訊息路徑與免疫系統調控的交互作用之研究

Project Coordinator/計畫主持人

Ming-Wei Lu

Funding Organization/主管機關

National Science and Technology Council

Department/Unit

Department of Aquaculture

Website

https://www.grb.gov.tw/search/planDetail?id=8343754

Year

2014

Start date/計畫起

01-08-2014

Expected Completion/計畫迄

31-07-2015

Bugetid/研究經費

1600千元

ResearchField/研究領域

漁業
生物技術(農)

"石斑魚養殖在台灣是養殖上重要的產業，而由於病毒性疾病普遍的肆虐，使得石斑魚疾病相關的研究工作成為近年來主要的研究焦點，不論於病理、檢測乃至疫苗開發都有豐碩的研究成果；然而在另一方面，我們對石斑魚免疫系統的認識到目前卻仍然非常地匱乏。在魚類先天免疫的研究方面，目前已經知道有某些機制與哺乳類十分不同，例如魚類的 TRIF缺少了與 TRAF6結合的能力，顯示可能無法進行 IRF3/7路徑，但結果卻能活化下游干擾素的表現，這類型的研究對於免疫演化上的了解十分重要。本計畫擬研究 JAK-STAT訊息路徑與先天免疫系統調控之間的關係，同時探討石斑魚在對抗病毒感染時免疫系統的反應且進一步確認 SOCS3在持續性感染模式下扮演的角色；我們先前已於馬拉巴石斑魚上選殖出 STAT1轉錄蛋白之全長基因，並且確認其遭受神經壞死病毒的感染時，STAT1在抗病毒免疫反應中扮演相當重要的角色；而在本計畫我們擬進一步以 NNV作為感染模式研究石斑魚的 STAT2至 STAT6對於其下游的干擾素誘發基因(ISG)調控的功能差異；另外將研究 JAK-STAT的負向調節 (SOCS3)對於 NNV 感染後造成的持續性感染相關性，但是這些機制在魚類免疫上的研究仍然非常不足，期望本計畫之完成將有對於石斑魚的抵抗病毒感染與 NNV造成的免疫弱化機制之瞭解有所幫助。 " "Aquaculture of grouper is an important and profitable industry in Taiwan. However, due to the widespread viral disease of grouper, the research on epidemic prevention or control has become important issue in period of years. The studies on viral pathogenesis, pathogen detection and vaccine development all carried out plenty achievements. But on the other side, the knowledge about grouper immune system is still lacking. There are some differences of innate immunity between fish and mammal system. For example, the fish TRIF could not bind to TRAF6, which implied could not activate IRF3/7 pathway. However the downstream IFN gene still expressed. In this proposal we planned to focus on the relationship between JAK-STAT signaling and innate immune system regulation, then further confirm the role of SOCS3 in grouper which infected by NNV persistent infection. In our previous study, we found the STAT1 is an important role in anti-viral immune response on grouper. Hence, in this proposal we will further characterize STAT2 to STAT3 respectively and their effects on downstream interferon stimulate gene (ISG) while NNV infection. Another negative regulation pathway is SOSC3, which major suppresses JAK-STAT pathway. According to prior related studies, we suspect the suppression of JAK-STAT by SOCS3 may play a crucial role in NNV persistent infection on grouper. But most of these mechanisms are still not clear. For this reason, we expect we could obtain more information about the mechanism of anti-viral immune and NNV persistent infection after finishing this project. "

Keyword(s)

先天免疫
石斑魚
訊息傳遞及轉錄活化因子
Innate immunity
Grouper
STAT

DSpace CRIS

The Interaction between JAK-STAT Signalling and Immune Regulation in Grouper

基本資料

Description