최진용 이학박사
부교수
가톨릭대학교 의과대학 미생물학교실
가톨릭대학교 대학원 의과학과
Jinyong Choi, Ph.D.
Associate Professor
Department of Microbiology,
College of Medicine, The Catholic University of Korea
Department of Medical Sciences, Graduate School of The Catholic University of Korea
ORCiD: 0000-0003-2474-2837
Jinyong Choi, Ph.D., studies the intricate molecular mechanisms that regulate immune responses in various physiological and pathological conditions. Specifically, we investigate the function of follicular helper T (TFH) cells, transcription factors, and their downstream targets in the context of infection, vaccination, and immunological disorders, such as autoimmune diseases, allergies, and even cancers.
Our research aims to unravel the complex interactions between these key transcription factors and downstream targets, with the goal of identifying novel therapeutic targets and approaches for the treatment of immunological diseases. By using cutting-edge techniques such as transcriptomic analysis, epigenetics analysis, gene editing, and mouse animal models, we strive to understand better the underlying molecular mechanisms that regulate immune responses.
T follicular helper (TFH) cells are a distinct subset of CD4+ T cells that play a critical role in generating effective humoral immunity. They are essential for the formation of germinal centers (GCs), affinity maturation of GC B cells, differentiation of high-affinity antibody-producing plasma cells, and the generation of memory B cells. The dysregulation of TFH cells has been implicated in a range of diseases, and thus, understanding the molecular mechanisms underlying TFH cell regulation is of great importance.
Our laboratory primarily focuses on regulating the differentiation and function of TFH by the transcription factors, including B cell lymphoma 6 (Bcl6), which is the lineage-defining factor of TFH cells. Our research aims to decipher the complex gene regulatory networks orchestrated by Bcl6 and other transcription factors contributing to TFH biology.
Research Areas:
Modulation of TFH by Bcl6 and other transcription factors:
We aim to uncover additional transcription factors contributing to TFH biology, focusing on their modulation of TFH functions and their interactions with Bcl6.
Repressor-of-repressor gene circuits:
Bcl6, as an obligate repressor, might control non-TFH and TFH genes by at least two repressor modes of action: (i) direct repression; and (ii) repression-of-repressor mechanisms. Blimp1 (encoded by Prdm1) is an excellent example of a repressor-of-repressor circuit. There is a reciprocal antagonistic relationship between Bcl6 and Blimp1; Bcl6 represses Prdm1, and Blimp1 represses Bcl6. The other examples are Id2, Runx3, and Klf2. Our research explores the multiple repressor-of-repressor gene circuits through which Bcl6 controls pleiotropic attributes of TFH differentiation and function.
Bcl6 negative autoregulation:
As shown in B cells, Bcl6 exhibits direct negative autoregulatory feedback in TFH cells. We investigate the negative autoregulation of Bcl6 and its impact on TFH biology, including migration, costimulation, inhibitory receptors, and cytokines.
Further readings:
Kim YJ#, Choi J#, and Choi YS. Transcriptional Regulation of Tfh Dynamics and Formation of Immunological Synapse. Experimental & Molecular Medicine, 2024; 56:1365-1372
Choi J* and Crotty S*. Bcl6-Mediated Transcriptional Regulation of Follicular Helper T cells (TFH). Trends in Immunology, 2021;42(4):336-349
Choi J, Diao H, Faliti CE, Truong J, Rossi M, Bélanger S, Yu B, Goldrath AW, Pipkin ME, and Crotty S. Bcl-6 is the nexus transcription factor of T follicular helper cell differentiation via repressor-of-repressor gene circuits. Nature Immunology, 2020;21(7):777-789
By advancing our understanding of TFH biology and Bcl6-mediated gene regulation, we hope to provide insights into biomedically relevant diseases and inform potential therapeutic strategies.
Research Areas:
Infection
Vaccines
Autoimmune Diseases
Allergy
Cancers
Through our multidisciplinary approach, we strive to uncover the complex gene regulatory networks that govern TFH cell differentiation and function, ultimately leading to a deeper understanding of the role of these cells in immune responses and disease pathogenesis.
Kim YJ#, Choi J#, and Choi YS. Transcriptional Regulation of Tfh Dynamics and Formation of Immunological Synapse. Experimental & Molecular Medicine, 2024; 56:1365-1372 #Equally contributed.
Choi J*, Crotty S, and Choi YS*. Cytokines in Follicular Helper T Cell Biology in Physiologic and Pathologic Conditions. Immune Network, 2024;24(1):e8 *Co-corresponding authors
Wi T, Choi Y, Kim J, Choi YS, Pipkin ME, and Choi J. Efficient gene deletion of Integrin alpha 4 in primary mouse CD4 T cells using CRISPR RNA pair-mediated fragmentation. Frontiers in Immunology. 2024; 15:1445341
Yoon M, Choi Y, Wi T, Choi YS, and Choi J. The role of cGAMP via the STING pathway in modulating germinal center responses and CD4 T cell differentiation. Frontiers in Immunology. 2024; 15:1340001
Choi J* and Crotty S*. Bcl6-Mediated Transcriptional Regulation of Follicular Helper T cells (TFH). Trends in Immunology, 2021;42(4):336-349
*Co-corresponding authors (Cited 180 as of Sep 2026)
Choi J, Diao H, Faliti CE, Truong J, Rossi M, Bélanger S, Yu B, Goldrath AW, Pipkin ME, and Crotty S. Bcl-6 is the nexus transcription factor of T follicular helper cell differentiation via repressor-of-repressor gene circuits. Nature Immunology, 2020;21(7):777-789 (Cited 157 as of Sep 2025)
2024. 6. 3. 한빛사 논문 소개
2022. 4. 8. Jinyong received NIH P01 subaward.
2021. 3. 4. 한빛사 논문 소개
2020. 6. 24. 한빛사 논문 소개
We are dedicated to fostering a collaborative and innovative research environment that promotes scientific discovery and translation of our findings into clinical research. We welcome collaborations and partnerships with other researchers, clinicians, and industry partners who share our commitment to advancing the field of immunology and improving patient outcomes.
박사 후 연구원, 박사 학위 과정, 석/박통합 학위 과정 대학원생 모집 중입니다. 아래 연락처로 문의바랍니다.
서울특별시 서초구 반포대로 222 가톨릭대학교 의과대학
옴니버스파크 의과대학동 8132호 (실험실 8108호)
