Sang‐Jun Ha
Yonsei University · Medicine
Sang-Jun Ha 교수의 연구실은 만성 바이러스 감염, 특히 HIV, B형 및 C형 간염 바이러스와 같은 지속성 감염에서 T세포 기능 부전을 해결하기 위한 면역치료 전략을 개발하고 있습니다. 주로 PD-1/PD-L1 억제와 IL-12/IL-23 시스템을 활용한 백신 부스터 전략, 그리고 T세포의 기능적 피로를 회복시키는 면역조절 기전을 중심으로 연구를 진행하고 있습니다. 특히, IL-12p40의 이중 기능과 IL-23이 유도하는 강력한 Th1 및 세포용해성 T세포 반응을 규명함으로써, 만성 감염 치료를 위한 새로운 백신 전략의 기초를 마련하고 있습니다.
Figures are computed from collected data and may differ slightly.
Therapeutic vaccination is a potentially promising strategy to enhance T cell immunity and viral control in chronically infected individuals. However, therapeutic vaccination approaches have fallen short of expectations, and effective boosting of antiviral T cell responses has not always been observed. One of the principal reasons for the limited success of therapeutic vaccination is that virus-specific T cells become functionally exhausted during chronic infections. We now provide a novel strat
IL-12p70 plays a pivotal role in regulating the Th1/Th2 balance in the initial stage of immune responses. In contrast, IL-12p40, which is produced excess over IL-12p70, has been known to down-regulate IL-12p70-mediated responses by acting as an antagonist. To investigate in vivo function of IL-12p40, RH7777 rat hepatoma cells were engineered to inducibly express mouse IL-12p40 under the tight control of doxycycline (dox). In the absence of dox, s.c. injection of these cells into syngeneic rat wa
One potentially promising strategy to control chronic infections such as human immunodeficiency virus, hepatitis B virus, and hepatitis C virus is therapeutic vaccination, which aims to reduce persisting virus by stimulating a patient's own antiviral immune responses. However, this approach has fallen short of expectations, because antiviral T cells generated during chronic infections often become functionally exhausted and thus do not respond properly to therapeutic vaccination. Therefore, it i
IL-23 is a heterodimeric cytokine consisting of p19 and the p40 subunit of IL-12. IL-23 has been shown to possess IL-12-like biological activities, but is different in its capacity to stimulate memory T cells in vitro. In this study, we investigated whether IL-23 could influence envelope protein 2 (E2)-specific cell-mediated immunity induced by immunization of hepatitis C virus E2 DNA. We found that IL-23 induced long-lasting Th1 and CTL immune responses to E2, which are much stronger than IL-12
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