Publications by authors named "Seongji Han"

Wheels have been commonly used for locomotion in mobile robots and transportation systems because of their simple structure and energy efficiency. However, the performance of wheels in overcoming obstacles is limited compared with their advantages in driving on normal flat ground. Here, we present a variable-stiffness wheel inspired by the surface tension of a liquid droplet.

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  • Males and females have different immune systems, but it's not clear why.
  • Researchers found that certain immune cells, called ILC2s, help explain these sexual differences in skin immunity.
  • The study suggests that male hormones reduce the number of important immune cells, affecting how well males can fight off diseases.
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Skin-resident CD8 T cells include distinct interferon-γ-producing [tissue-resident memory T type 1 (T1)] and interleukin-17 (IL-17)-producing (T17) subsets that differentially contribute to immune responses. However, whether these populations use common mechanisms to establish tissue residence is unknown. In this work, we show that T1 and T17 cells navigate divergent trajectories to acquire tissue residency in the skin.

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  • - Mild dietary restriction (DR) improves health and immune responses, specifically by optimizing memory T cells and their interactions with myeloid cells in fighting infections.
  • - DR promotes the growth of beneficial gut bacteria like Bifidobacteria, which produce acetate that enhances myeloid cell function against pathogens.
  • - The effectiveness of DR on immunity relies on a healthy gut microbiota, illustrating how nutrition influences immune cooperation and response to infections.
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The microbiota performs multiple functions vital to host fitness, including defense against pathogens and adaptation to dietary changes. Yet, how environmental challenges shape microbiota resilience to nutrient fluctuation remains largely unexplored. Here, we show that transient gut infection can optimize host metabolism toward the usage of carbohydrates.

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Tissue immunity and responses to injury depend on the coordinated action and communication among physiological systems. Here, we show that, upon injury, adaptive responses to the microbiota directly promote sensory neuron regeneration. At homeostasis, tissue-resident commensal-specific T cells colocalize with sensory nerve fibers within the dermis, express a transcriptional program associated with neuronal interaction and repair, and promote axon growth and local nerve regeneration following injury.

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Immune checkpoint inhibitors (ICIs) are essential components of the cancer therapeutic armamentarium. While ICIs have demonstrated remarkable clinical responses, they can be accompanied by immune-related adverse events (irAEs). These inflammatory side effects are of unclear etiology and impact virtually all organ systems, with the most common being sites colonized by the microbiota such as the skin and gastrointestinal tract.

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  • Maternal infections during pregnancy can permanently affect the immune system of offspring in tissue-specific ways.
  • The cytokine interleukin-6, produced by mothers in response to infections, can trigger epigenetic changes in fetal intestinal cells.
  • Offspring of infected mothers may have better protection against gut infections but could also be more prone to inflammatory disorders like colitis.
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The microbiota plays a fundamental role in regulating host immunity. However, the processes involved in the initiation and regulation of immunity to the microbiota remain largely unknown. Here, we show that the skin microbiota promotes the discrete expression of defined endogenous retroviruses (ERVs).

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  • The immune system is always prepared to recognize and respond to the microbiota, which includes a preexisting pool of T cells specific to these microorganisms, even before any inflammatory trigger occurs.
  • In a study using a psoriasis model, exposure to certain commensal skin fungi was found to worsen tissue inflammation due to pre-formed T cell responses.
  • The increased inflammation linked to fungal exposure involves specific immune mechanisms (Th17 responses and neutrophil traps) and shares similarities with the gene expression patterns seen in human psoriasis-affected skin.
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The cross-talk between the microbiota and the immune system plays a fundamental role in the control of host physiology. However, the tissue-specific factors controlling this dialogue remain poorly understood. Here we demonstrate that T cell responses to commensal colonization are associated with the development of organized cellular clusters within the skin epithelium.

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How early-life colonization and subsequent exposure to the microbiota affect long-term tissue immunity remains poorly understood. Here, we show that the development of mucosal-associated invariant T (MAIT) cells relies on a specific temporal window, after which MAIT cell development is permanently impaired. This imprinting depends on early-life exposure to defined microbes that synthesize riboflavin-derived antigens.

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  • Mammals developed their immune system in response to changing food availability, but how it adapts during periods of restricted nutrition is not well understood.
  • Research shows that during dietary restriction, memory T cells decrease in secondary lymphoid organs but increase significantly in the bone marrow, where they enter an energy-conserving state.
  • This shift, influenced by stress hormones and changes in the bone marrow, helps maintain immune memory and improve protection against infections and tumors.
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Laboratory mouse studies are paramount for understanding basic biological phenomena but also have limitations. These include conflicting results caused by divergent microbiota and limited translational research value. To address both shortcomings, we transferred C57BL/6 embryos into wild mice, creating "wildlings.

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  • Barrier tissues, like the skin, are important for immune defense and contain many immune cells called commensal-specific T cells, which respond to environmental stressors.
  • These skin-resident T cells exhibit a unique dual program that allows them to quickly switch to a tissue-repairing mode when faced with injury or inflammation.
  • However, if the immune regulation is disrupted, these T cells can also trigger harmful overreactions, highlighting their role in balancing local immunity and tissue healing.
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  • - The research highlights how the immune system senses and responds to the microbiota on skin barrier surfaces, focusing on T cell responses that utilize non-classical MHC class I molecules.
  • - These commensal-specific T cells, which are different from pathogen-induced immune cells, play a role in promoting protection against pathogens and enhancing skin wound healing.
  • - The findings suggest that non-classical MHC class I molecules contribute to a unique form of adaptive immunity that integrates anti-microbial functions with tissue repair, showing their importance in maintaining homeostasis with the microbiota.
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  • White adipose tissue (WAT) is essential for body metabolism and may play a significant role in immune defense, though this is not fully understood.
  • Researchers found that WAT contains large populations of memory lymphocytes and accumulates pathogen-specific memory T cells after infection.
  • The study indicates that WAT produces a rapid immune response by hindering lipid metabolism to enhance antimicrobial functions, suggesting it could be a key player in immunological memory.
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  • Infections, particularly from agents like Yersinia pseudotuberculosis, can lead to lasting tissue-specific immune system changes following clearance.
  • * After an acute infection, inflammation and lymphatic issues in the mesenteric adipose tissue can divert immune cells away from where they're needed, hindering key immune functions.
  • * Signals from the body's microbiota keep this inflammatory state going, but removing the microbiota can temporarily restore immune function, highlighting how infections can have long-term effects on immune health.
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  • Tissue-infiltrating Ly6C(hi) monocytes play key roles in immune responses, but their diverse functions and how they develop are not fully understood.
  • During acute gastrointestinal infections, these monocytes are primed for regulatory roles before systemic inflammation begins, with this process starting in the bone marrow.
  • The study highlights that NK cell-derived IFN-γ, influenced by IL-12 from dendritic cells, helps shape monocyte development in the bone marrow rather than just their post-recruitment function in tissues.
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  • The skin acts as a critical barrier between the body and the environment, hosting trillions of microorganisms that help maintain tissue health and immunity.
  • Recent research shows that specific beneficial microbes, like Staphylococcus epidermidis, can influence skin immunity by promoting certain immune cells that enhance defense mechanisms against pathogens.
  • This study highlights the complex interactions between skin-resident cells and commensal microorganisms, suggesting that these relationships can adapt quickly to changing microbial environments, which is important for understanding skin immunity and related health issues.
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The classic anti-viral cytokine interferon (IFN)-β can be induced during parasitic infection, but relatively little is know about the cell types and signaling pathways involved. Here we show that inflammatory monocytes (IMs), but not neutrophils, produce IFN-β in response to T. gondii infection.

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Toxoplasma gondii infection occurs through the oral route, but we lack important information about how the parasite interacts with the host immune system in the intestine. We used two-photon laser-scanning microscopy in conjunction with a mouse model of oral T. gondii infection to address this issue.

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Infection leads to heightened activation of natural killer (NK) cells, a process that likely involves direct cell-to-cell contact, but how this occurs in vivo is poorly understood. We have used two-photon laser-scanning microscopy in conjunction with Toxoplasma gondii mouse infection models to address this question. We found that after infection, NK cells accumulated in the subcapsular region of the lymph node, where they formed low-motility contacts with collagen fibers and CD169(+) macrophages.

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Clearance of infection with intracellular pathogens in mice involves interferon-regulated GTPases of the IRG protein family. Experiments with mice genetically deficient in members of this family such as Irgm1(LRG-47), Irgm3(IGTP), and Irgd(IRG-47) has revealed a critical role in microbial clearance, especially for Toxoplasma gondii. The in vivo role of another member of this family, Irga6 (IIGP, IIGP1) has been studied in less detail.

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Cell death is an important mechanism to limit uncontrolled T-cell expansion during immune responses. Given the role of death-receptor adapter protein Fas-associated death domain (FADD) in apoptosis, it is intriguing that T-cell receptor (TCR)-induced proliferation is blocked in FADD-defective T cells. Necroptosis is an alternate form of death that can be induced by death receptors and is linked to autophagy.

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