Publications by authors named "Yuji Nagano"

Article Synopsis
  • Pulmonary fibrosis (PF) is a lung disease that makes it hard to breathe and can be life-threatening.
  • Scientists discovered that certain mice (Ifngr1Rag2) that lack a key suppressor for immune cells called ILC2 can develop PF on their own.
  • The study shows that these ILC2 cells produce a protein that makes fibroblasts (cells that help with tissue repair) create too much collagen, causing the lungs to become stiff and fibrous.
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Group 2 innate lymphoid cells (ILC2s) expressing IL-5 and IL-13 are localized at various mucosal tissues and play critical roles in the induction of type 2 inflammation, response to helminth infection, and tissue repair. Here, we reveal a unique ILC2 subset in the mouse intestine that constitutively expresses IL-4 together with GATA3, ST2, KLRG1, IL-17RB, and IL-5. In this subset, IL-4 expression is regulated by mechanisms similar to but distinct from those observed in T cells and is partly affected by IL-25 signaling.

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CD4(+) T cells that express the forkhead box P3 (FOXP3) transcription factor function as regulatory T (Treg) cells and hinder effective immune responses against cancer cells. Abundant Treg cell infiltration into tumors is associated with poor clinical outcomes in various types of cancers. However, the role of Treg cells is controversial in colorectal cancers (CRCs), in which FOXP3(+) T cell infiltration indicated better prognosis in some studies.

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Article Synopsis
  • Intestinal Th17 cells are stimulated and increase in number when specific gut microbes, like segmented filamentous bacteria (SFB), colonize the gut, especially during interactions with certain pathogens.
  • The adhesion of these microbes to intestinal epithelial cells (ECs) is crucial for the induction of Th17 cells, as only bacteria that attach effectively can trigger this immune response in germ-free mice or rats.
  • A diverse group of 20 bacterial strains linked to ulcerative colitis were found to not only induce Th17 cells but also demonstrate strong adherence to ECs, highlighting the importance of bacterial adhesion in immune responses.
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Manipulation of the gut microbiota holds great promise for the treatment of inflammatory and allergic diseases. Although numerous probiotic microorganisms have been identified, there remains a compelling need to discover organisms that elicit more robust therapeutic responses, are compatible with the host, and can affect a specific arm of the host immune system in a well-controlled, physiological manner. Here we use a rational approach to isolate CD4(+)FOXP3(+) regulatory T (Treg)-cell-inducing bacterial strains from the human indigenous microbiota.

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Foxp3+ CD4+ cells are prominent immune regulatory T (Treg) cells that are most abundant in the intestine. Recent studies have suggested that intestinal Treg cells consist of thymically and extrathymically developed cells that have unique characteristics. A fraction of intestinal Treg cells express T cell receptors that recognize antigens that are derived from the gut microbiota.

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