Yonsei University · 医学
Professor June-Yong Lee's research lab focuses on immune regulation, particularly the development and function of regulatory T cells (Tregs) and T helper 17 (Th17) cells in mucosal immunity and systemic inflammation. The lab investigates how environmental and microbial signals, including thymic stromal lymphopoietin (TSLP) and the microbiota, shape T cell fate decisions and maintain immune homeostasis. Key research directions include the transcriptional regulation of T cell subsets, the role of innate-like memory CD8 T cells in infection and immunity, and the impact of metabolic inflammation in obesity and autoimmune diseases.
Figures are computed from collected data and may differ slightly.
Previous studies revealed the existence of foreign antigen-specific memory phenotype CD8 T cells in unimmunized mice. Considerable evidence suggests this population, termed "virtual memory" (VM) CD8 T cells, arise via physiological homeostatic mechanisms. However, the antigen-specific function of VM cells is poorly characterized, and hence their potential contribution to immune responses against pathogens is unclear. Here we show that naturally occurring, polyclonal VM cells have unique function
Specification of endothelial cell (EC) fate during vascular development is controlled by distinct key regulators. While Notch plays an essential role in induction of arterial phenotypes, COUP-TFII is required to maintain the venous EC identity. Homeodomain transcription factor Prox1 functions to reprogram venous ECs to lymphatic endothelial cells (LECs). Here, we report that the venous EC fate regulator COUP-TFII is expressed in LECs throughout development and physically interacts with Prox1 to
T helper 17 (Th17) cells regulate mucosal barrier defenses but also promote multiple autoinflammatory diseases. Although many molecular determinants of Th17 cell differentiation have been elucidated, the transcriptional programs that sustain Th17 cells in vivo remain obscure. The transcription factor RORγt is critical for Th17 cell differentiation; however, it is not clear whether the closely related RORα, which is co-expressed in Th17 cells, has a distinct role. Here, we demonstrated that altho
The human gastrointestinal tract has an enormous and diverse microbial community, termed microbiota, that is necessary for the development of the immune system and tissue homeostasis. In contrast, microbial dysbiosis is associated with various inflammatory and autoimmune diseases as well as neurological disorders in humans by affecting not only the immune system in the gastrointestinal tract but also other distal organs. FOXP3<sup>+</sup> regulatory T cells (Tregs) are a subset of CD4<sup>+</sup
Human thymic stromal lymphopoietin (TSLP) activates dendritic cells (DCs), which promote the proliferation and differentiation of CD4+ T cells. However, murine TSLP (mTSLP) can act directly on CD4+ T cells and bring about their differentiation. We studied the role of mTSLP in the generation of CD4+CD25+FoxP3+ T cells from thymocytes. mTSLP promoted the differentiation of CD4+ single-positive thymocytes into CD4+CD25+FoxP3+ T cells. Although we cannot exclude an effect of TSLP mediated through DC
Obesity is a chronic inflammatory state and adipose tissue serves as a source of inflammatory mediators. This study compared plasma levels of the proinflammatory cytokines interleukin-6 (IL-6) and tumour necrosis factor-α (TNF-α) in 20 morbidly obese patients (group O) undergoing laparoscopic Roux-en-Y gastric bypass surgery and in 20 non-obese control patients (group C) undergoing laparascopic gastrectomy. Blood was sampled preoperatively and at 3 and 24 h postoperatively. Postoperative IL-6 le
Summary T helper 17 (Th17) cells regulate mucosal barrier defenses, but also promote multiple autoinflammatory diseases. Although many molecular determinants of Th17 cell differentiation have been described, the transcriptional programs that sustain Th17 cells in vivo remain obscure. The transcription factor RORγt is critical for Th17 cell differentiation, but a distinct role of the closely-related RORα, which is co-expressed in Th17 cells, is not known. Here we demonstrate that, although dispen
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