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학술연구/단체지원/교육 등 연구자 활동을 지속하도록 DBpia가 지원하고 있어요.
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연구자들이 자신의 연구와 전문성을 널리 알리고, 새로운 협력의 기회를 만들 수 있는 네트워킹 공간이에요.
논문 기본 정보
- 자료유형
- 학술대회자료
- 저자정보
- 발행연도
- 2010.2
- 수록면
- 89 - 93 (5page)
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Today, chronic viral infections such as HIV, HBV, and HCV, became a major issue to threaten public health. Chronically infected individuals not only act as a reservoir for viral spread, but also chronic infection in general increases the risk of subsequent diseases and secondary infections with other pathogens. In the face of continuously spreading viruses, there is an urgent need to develop vaccines that can be used therapeutically. Many chronic viral infections are marked by pathogen persistence and a generalized immunosuppression. The exact mechanisms by which this occurs are still unknown. The strategy comparing immune responses after acute vs. chronic viral infection might be one of the ways to uncover the mechanism of immunosuppression caused by chronic viral infection. We analyzed the function and phenotype of both T cells and dendritic cells (DCs) after acute vs. chronic infection. By comparing antigen-specific acute and chronic T cells, we found that co-inhibitory molecules including Programmed death 1 (PD-1) are highly expressed on T cells, suppress their function, and finally leads to a progressive exhaustion. We also observed that conversion of DC subtypes priming T cells (from lymphoid DCs to myeloid or plasmacytoid DCs) occurred during chronic infection but not acute infection. Therefore, the strategy both blocking inhibitory signals on T cells and targeting antigen to proper DCs might overcome immunosuppression and subsequently enhance the clearance of persistent virus.
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UCI(KEPA) : I410-ECN-0101-2010-510-002595251