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慶應医学会例会
下記により例会を開催いたしますので、多数ご来聴ください。
2025年1月28日（火） 17:00 開催
場 所
臨床研究棟1階 ラウンジ
演 題
Gynecologic Clinicians and Translational Research
Masaki Mandai MD, PhD
Department of Gynecology and Obstetrics, Graduate School of Medicine, Kyoto University
Department of Gynecology and Obstetrics, Graduate School of Medicine, Kyoto University
The term translational research has been in use for over 25 years and become a familiar concept in clinical practice. However, its perception often remains narrowly focused on drug development as a typical example, leading many clinicians to associate it primarily with large-scale clinical trials conducted by specialized experts.
In reality, translational research encompasses the process of applying diverse scientific discoveries to address unmet clinical needs. This broader understanding reveals that translational research does not necessarily require grand-scale endeavors; rather, it can be pursued more accessible by clinicians who recognize its potential.
I aim to share our initiatives and reflect on how gynecological clinicians-particularly younger practitioners-can engage in translational research more effectively.
In reality, translational research encompasses the process of applying diverse scientific discoveries to address unmet clinical needs. This broader understanding reveals that translational research does not necessarily require grand-scale endeavors; rather, it can be pursued more accessible by clinicians who recognize its potential.
I aim to share our initiatives and reflect on how gynecological clinicians-particularly younger practitioners-can engage in translational research more effectively.
担 当
産婦人科学 教室
責任者：田中 守 教授
担当者：山田 満稔 教授（内線 62381）
責任者：田中 守 教授
担当者：山田 満稔 教授（内線 62381）
2025年2月5日（水） 10:00 開催
場 所
2号館 中会議室
演 題
Unleashing cGAS-STING signaling to promote cancer immunogenicity
David A Barbie M.D.
Dana Farber Cancer Institute
Dana Farber Cancer Institute
担 当
呼吸器内科学 教室
責任者：福永 興壱 教授
担当者：寺井 秀樹 先生（内線 61424）
責任者：福永 興壱 教授
担当者：寺井 秀樹 先生（内線 61424）
2025年4月28日（月）18:00 開催
場 所
未定
演 題
Epstein-Barr Virus is Targeted by Converging T and B Cell Responses in Primary Sclerosing Cholangitis
Tom Hemming Karlsen M.D. PhD.
University of Oslo
University of Oslo
The cause of primary sclerosing cholangitis (PSC) is unknown, yet multiple studies have implicated different human leukocyte antigen (HLA) genetic variants in disease development. Other studies have shown alterations in T cell responses of people with PSC. We aimed for an integrated analyses of adaptive immune responses in PSC by comprehensive profiling of the blood T cell repertoire of 504 individuals with PSC and 904 healthy controls along with profiling of the functional antibody repertoire of 120 individuals with PSC and 202 matching healthy controls using phage-immunoprecipitation sequencing (PhIP-Seq). In follow up to the molecular data, we queried the health care records of individuals in the TriNetX database for disease associations.
Results: Using a hypothesis-free statistical analysis framework, we identified 1,008 T cell clonotypes that were associated with PSC. These clonotypes were mostly restricted to PSC-risk HLA variants such as the HLA-B*08:01-HLA-DRB1*03:01 haplotype as well as HLA-DRB1*13:01 and were shown to target different Epstein-Barr virus (EBV) epitopes, particularly, lytic-phase antigens such as BZLF1. Furthermore, for the PhIP-Seq data we detected elevated antibody responses toward different EBV lytic-phase antigens, predominantly the BMRF1 protein. In the TriNetX database, we detected a robust association between infectious mononucleosis, which is mainly caused by EBV, and PSC (odds ratio [OR]=8.46; 95% CI: 4.53-15.80).
Conclusion: We report for the first time that in PSC there are expanded T and B cell responses against EBV. Furthermore, these responses were predominantly detected for lytic-phase antigens which may indicate that EBV-reactivation is a central theme in the pathogenesis of PSC. Whilst similar findings have been reported for multiple sclerosis, the OR for the association between PSC and infectious mononucleosis was more than 4-fold higher than that found for multiple sclerosis.
Results: Using a hypothesis-free statistical analysis framework, we identified 1,008 T cell clonotypes that were associated with PSC. These clonotypes were mostly restricted to PSC-risk HLA variants such as the HLA-B*08:01-HLA-DRB1*03:01 haplotype as well as HLA-DRB1*13:01 and were shown to target different Epstein-Barr virus (EBV) epitopes, particularly, lytic-phase antigens such as BZLF1. Furthermore, for the PhIP-Seq data we detected elevated antibody responses toward different EBV lytic-phase antigens, predominantly the BMRF1 protein. In the TriNetX database, we detected a robust association between infectious mononucleosis, which is mainly caused by EBV, and PSC (odds ratio [OR]=8.46; 95% CI: 4.53-15.80).
Conclusion: We report for the first time that in PSC there are expanded T and B cell responses against EBV. Furthermore, these responses were predominantly detected for lytic-phase antigens which may indicate that EBV-reactivation is a central theme in the pathogenesis of PSC. Whilst similar findings have been reported for multiple sclerosis, the OR for the association between PSC and infectious mononucleosis was more than 4-fold higher than that found for multiple sclerosis.
担 当
内科学（消化器） 教室
責任者：金井 隆典 教授
担当者：中本 伸宏 先生（内線 62384）
責任者：金井 隆典 教授
担当者：中本 伸宏 先生（内線 62384）
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