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RISS 인기검색어
- 검색키워드
- 저자 : David B. Weiner (검색결과 4 건)
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David B. Weiner,신정임 대한면역학회 2005 Immune Network Vol.5 No.2
Background: Costimulation is a critical process in Ag-specific immune responses. Both B7.1 and CD28 molecules have been reported to stimulate T cell responses during antigen presentation. Therefore, we tested whether Ag-specific immune responses as well as protective immunity are influenced by coinjecting with B7.1 and CD28 cDNAs in a mouse HSV-2 challenge model system. Methods: ELISA was used to detect levels of antibodies, cytokines and chemokines while thymidine incorporation assay was used to evaluate T cell proliferation levels. Results: Ag-specific antibody responses were enhanced by CD28 coinjection but not by B7.1 coinjection. Furthermore, CD28 coinjection increased IgG1 production to a significant level, as compared to pgD pcDNA3, suggesting that CD28 drives Th2 type responses. In contrast, B7.1 coinjection showed the opposite, suggesting a Th1 bias. B7.1 coinjection also enhanced Ag-specific Th cell proliferative responses as well as production of Th1 type cytokines and chemokines significantly higher than pgD pcDNA3. However, CD28 coinjection decreased Ag-specific Th cell proliferative responses as well as production of Th1 types of cytokines and chemokine significantly lower than pgD pcDNA3. Only MCP-1 production was enhanced by CD28. B7.1 coimmunized animals exhibited an enhanced survival rate as well as decreased herpetic lesion formation, as compared to pgD pcDNA3. In contrast, CD28 vaccinated animals exhibited decreased survival from lethal challenge. Conclusion: This study shows that B7.1 enhances protective Th1 type cellular immunity against HSV-2 challenge while CD28 drives a more detrimental Th2 type immunity against HSV-2 challenge, supporting an opposite role of B7.1 and CD28 in Ag-specific immune responses to a Th1 vs Th2 type.
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Weiner, David B.,Sin, Jeong-Im The Korean Association of Immunobiologists 2005 Immune Network Vol.5 No.2
Background: Costimulation is a critical process in Ag-specific immune responses. Both B7.1 and CD28 molecules have been reported to stimulate T cell responses during antigen presentation. Therefore, we tested whether Ag-specific immune responses as well as protective immunity are influenced by coinjecting with B7.1 and CD28 cDNAs in a mouse HSV-2 challenge model system. Methods: ELISA was used to detect levels of antibodies, cytokines and chemokines while thymidine incorporation assay was used to evaluate T cell proliferation levels. Results: Ag-specific antibody responses were enhanced by CD28 coinjection but not by B7.1 coinjection. Furthermore, CD28 coinjection increased IgG1 production to a significant level, as compared to pgD+pcDNA3, suggesting that CD28 drives Th2 type responses. In contrast, B7.1 coinjection showed the opposite, suggesting a Th1 bias. B7.1 coinjection also enhanced Ag-specific Th cell proliferative responses as well as production of Th1 type cytokines and chemokines significantly higher than pgD+pcDNA3. However, CD28 coinjection decreased Ag-specific Th cell proliferative responses as well as production of Th1 types of cytokines and chemokine significantly lower than pgD+pcDNA3. Only MCP-1 production was enhanced by CD28. B7.1 coimmunized animals exhibited an enhanced survival rate as well as decreased herpetic lesion formation, as compared to pgD+pcDNA3. In contrast, CD28 vaccinated animals exhibited decreased survival from lethal challenge. Conclusion: This study shows that B7.1 enhances protective Th1 type cellular immunity against HSV-2 challenge while CD28 drives a more detrimental Th2 type immunity against HSV-2 challenge, supporting an opposite role of B7.1 and CD28 in Ag-specific immune responses to a Th1 vs Th2 type.
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( Ji Won Han ),( Pil Soo Sung ),( Seon-hui Hong ),( Hyojin Lee ),( Moonsup Jeong ),( Su-hyung Park ),( Jian Yan ),( Amir Khan ),( Joel N. Maslow ),( David B. Weiner ),( Jeong Heo ),( Sang Hoon Ahn ),( 대한간학회 2018 춘·추계 학술대회 (KASL) Vol.2018 No.1
Aims: Although direct-acting antivirals (DAA) are success fully used for the treatment of chronic hepatitis C, there are DAA-resistant cases. Furthermore, DAA-treated patients do not develop protective immunity against HCV re-infection. To complement DAA therapy, we developed a DNA vaccine (VGX- 6150) containing three plasmids encoding HCV genotype 1 NS3, NS4 and NS5A consensus immunogens and plasmid en coding IL-28B as a molecular adjuvant. In the present study, we performed a phase I clinical trial of VGX-6150 in patients with chronic hepatitis C (n=18) who had failed interferon (IFN)-based treatment. Methods: VGX-6150 was administered 4 times in 4-week in tervals with in vivo electroporation to three groups of patients (n=6 for 1, 3, and 6 mg/dose groups, respectively) followed by a 6 mg boost 24 weeks later. Significant side effects were not reported. Cellular immune responses of peripheral blood mono nuclear cells (PBMCs) were evaluated by IFN-g ELISpot assays using overlapping peptides spanning NS3~NS5A and staining with HCV-specific HLA class I pentamers. Results: The IFN-g spot number specific to NS3~NS5A was in creased in 3 and 6 mg/dose groups after the initial vaccination and in all three groups after the boosting vaccination. Howev er, the frequency of HCV-specific HLA class I pentamer+ CD8+ T-cells was not increased by the vaccination. Moreover, the fre quency of PD-1+ cells in the gate of HLA class I pentamer+ CD8+ T-cells was not changed by the vaccination. Interestingly, the frequency of CD4+CD25+Foxp3+ regulatory T-cells (Treg) was significantly decreased after the vaccination, consistent with a previous report regarding the effect of an IL-28B-encoding plasmid adjuvant. Conclusions: In the present study, we demonstrate that VGX- 6150 enhances HCV antigen-specific T-cell responses without significant side effects. The inclusion of IL-28B as an immune adjuvant was associated with a decrease in Treg cells that may have provided greater immune activation in chronic HCV infec- tion.
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