https://scholar.dgist.ac.kr/handle/20.500.11750/884 2026-04-04T16:56:44Z 2026-04-04T16:56:44Z Byun, Seohyun Lee, Jusung Choi, Yoon Ha Ko, Haeun Lee, Changhon Park, John Chulhoon Kim, Seung Won Lee, Haena Sharma, Amit Kim, Kwang Soon Rudra, Dipayan Kim, Jong Kyoung Im, Sin-Hyeog https://scholar.dgist.ac.kr/handle/20.500.11750/57447 2025-07-25T02:42:57Z 2024-08-31T15:00:00Z

Title: Gut Microbiota Defines Functional Direction of Colonic Regulatory T Cells with Unique TCR Repertoires Author(s): Byun, Seohyun; Lee, Jusung; Choi, Yoon Ha; Ko, Haeun; Lee, Changhon; Park, John Chulhoon; Kim, Seung Won; Lee, Haena; Sharma, Amit; Kim, Kwang Soon; Rudra, Dipayan; Kim, Jong Kyoung; Im, Sin-Hyeog Abstract: Intestinal microbiota and selected strains of commensal bacteria influence regulatory T (Treg) cell functionality in the colon. Nevertheless, whether and how microbiota changes the transcriptome profile and TCR specificities of colonic Tregs remain to be precisely defined. In this study, we have employed single-cell RNA sequencing and comparatively analyzed colonic Tregs from specific pathogen-free and germ-free (GF) mice. We found that microbiota shifts the activation trajectory of colonic Tregs toward a distinct phenotypic subset enriched in specific pathogen-free but not in GF mice. Moreover, microbiota induced the expansion of specific Treg clonotypes with shared transcriptional specificities. The microbiota-induced subset of colonic Tregs, identified as PD-12 CXCR3+ Tregs, displayed enhanced suppressive capabilities compared with colonic Tregs derived from GF mice, enhanced production of IL-10, and were the primary regulators of enteric inflammation in dextran sodium sulfate-induced colitis. These findings identify a hitherto unknown gut microbiota and immune cell interaction module that could contribute to the development of a therapeutic modality for intestinal inflammatory diseases. © 2024 by The American Association of Immunologists, Inc.

2024-08-31T15:00:00Z Kyung, Dong Soo Lee, Eun Min Chae, Sehyun Son, Yeonho Moon, Ye-Jin Hwang, Daehee Kim, Jong Kyoung Lee, Yun-Hee Seong, Je Kyung https://scholar.dgist.ac.kr/handle/20.500.11750/57410 2025-07-25T02:42:40Z 2024-09-30T15:00:00Z

Title: Single-cell transcriptomic analysis reveals dynamic activation of cellular signaling pathways regulating beige adipogenesis Author(s): Kyung, Dong Soo; Lee, Eun Min; Chae, Sehyun; Son, Yeonho; Moon, Ye-Jin; Hwang, Daehee; Kim, Jong Kyoung; Lee, Yun-Hee; Seong, Je Kyung Abstract: PDGFRA+ cells have been identified as adipocyte stem cells (ASCs) that differentiate into beige adipocytes in white adipose tissue (WAT) following thermogenic stimuli. To elucidate the molecular heterogeneity of ASCs, we conducted single-cell transcriptomic profiling of PDGFRA+ cells isolated from the inguinal WAT (iWAT) of mice treated with the beta3 adrenergic receptor agonist CL316243. Single-cell RNA-seq revealed nine major clusters, which were categorized into four groups: resting, proliferating, differentiating, and adipogenic factor-expressing cells (AFECs). Trajectory analysis revealed sequential activation of molecular pathways, including the Hedgehog and Notch signaling pathways, during beige adipogenesis. AFECs expressed Dpp4 and did not differentiate into adipocytes in culture or after transplantation. Furthermore, genetic lineage tracing studies indicated that DPP4+ cells did not differentiate into adipocytes in iWAT during CL316243-induced beige adipogenesis. However, high-fat diet feeding led to the recruitment of adipocytes from DPP4+ cells in iWAT. Overall, this study improved our understanding of the dynamic molecular basis of beige adipogenesis and the potential contribution of DPP4+ adipocyte lineages to the pathological expansion of WAT during diet-induced obesity. © The Author(s) 2024.

2024-09-30T15:00:00Z Jung, Sukjoon Kim, Hyunmin Lee, Juhyeon Kang, Myeong Hoon Kim, Jung Yeon Kim, Jong Kyoung Lim, Pyung Ok Nam, Hong Gil https://scholar.dgist.ac.kr/handle/20.500.11750/57390 2025-07-25T04:25:05Z 2024-10-31T15:00:00Z

Title: The genetically programmed rhythmic alteration of diurnal gene expression in the aged Arabidopsis leaves Author(s): Jung, Sukjoon; Kim, Hyunmin; Lee, Juhyeon; Kang, Myeong Hoon; Kim, Jung Yeon; Kim, Jong Kyoung; Lim, Pyung Ok; Nam, Hong Gil Abstract: The circadian clock regulates the daily pattern of temporal gene expression. In Arabidopsis, aging is associated with a shortening of the endogenous period of circadian rhythms under circadian conditions. However, the functional link between the circadian clock and aging under diurnal conditions and its physiological relevance remain elusive. In this study, we investigate and characterize the effect of aging on the waveforms of rhythmic gene expression patterns under light/dark cycles. Our analysis revealed that the diurnal rhythmic patterns of core clock genes undergo significant rhythmic alteration with phase shift and change of waveforms in aged plants compared to younger plants. Transcriptomic analysis indicated that this age-dependent rhythmic alteration occurs not only in core clock genes but also globally. Due to the rhythmic alteration patterns of the diurnal rhythmic gene expression, aged plants experience subjectively a shorter day and longer night. We also observed that genetic mutants of core clock component genes exhibited broadly yet distinctively altered changes in diurnal rhythmic gene expression patterns as aging progresses. Collectively, our findings support that age-dependent rhythmic alteration of diurnal gene expression rhythms reprograms the timetable of daily gene expression, leading to the physiological changes required for plant senescence. Copyright © 2024 Jung, Kim, Lee, Kang, Kim, Kim, Lim and Nam.

2024-10-31T15:00:00Z Sharma, Garima Sharma, Amit Kim, Inhae Cha, Dong Gon Kim, Somi Park, Eun Seo Noh, Jae Gyun Lee, Juhee Ku, Ja Hyeon Choi, Yoon Ha Kong, Jungho Lee, Haena Ko, Haeun Lee, Juhun Notaro, Anna Hong, Seol Hee Rhee, Joon Haeng Kim, Sang Geon De Castro, Cristina Molinaro, Antonio Shin, Kunyoo Kim, Sanguk Kim, Jong Kyoung Rudra, Dipayan Im, Sin-Hyeog https://scholar.dgist.ac.kr/handle/20.500.11750/57086 2025-07-25T02:41:12Z 2024-04-30T15:00:00Z

Title: A dietary commensal microbe enhances antitumor immunity by activating tumor macrophages to sequester iron Author(s): Sharma, Garima; Sharma, Amit; Kim, Inhae; Cha, Dong Gon; Kim, Somi; Park, Eun Seo; Noh, Jae Gyun; Lee, Juhee; Ku, Ja Hyeon; Choi, Yoon Ha; Kong, Jungho; Lee, Haena; Ko, Haeun; Lee, Juhun; Notaro, Anna; Hong, Seol Hee; Rhee, Joon Haeng; Kim, Sang Geon; De Castro, Cristina; Molinaro, Antonio; Shin, Kunyoo; Kim, Sanguk; Kim, Jong Kyoung; Rudra, Dipayan; Im, Sin-Hyeog Abstract: Here the authors show that a heteropolysaccharide from a commensal bacteria commonly found in the Korean food kimchi is able to bolster antitumor immune responses by instructing tumor-associated macrophages to release lipocalin-2, which sequesters iron away from tumor cells contributing to the immune response to attack these cells. © The Author(s), under exclusive licence to Springer Nature America, Inc. 2024.. Innate immune cells generate a multifaceted antitumor immune response, including the conservation of essential nutrients such as iron. These cells can be modulated by commensal bacteria; however, identifying and understanding how this occurs is a challenge. Here we show that the food commensal Lactiplantibacillus plantarum IMB19 augments antitumor immunity in syngeneic and xenograft mouse tumor models. Its capsular heteropolysaccharide is the major effector molecule, functioning as a ligand for TLR2. In a two-pronged manner, it skews tumor-associated macrophages to a classically active phenotype, leading to generation of a sustained CD8+ T cell response, and triggers macrophage ‘nutritional immunity’ to deploy the high-affinity iron transporter lipocalin-2 for capturing and sequestering iron in the tumor microenvironment. This process induces a cycle of tumor cell death, epitope expansion and subsequent tumor clearance. Together these data indicate that food commensals might be identified and developed into ‘oncobiotics’ for a multi-layered approach to cancer therapy. © The Author(s), under exclusive licence to Springer Nature America, Inc. 2024.

2024-04-30T15:00:00Z