Pohang University of Science and Technology · Biochemistry, Genetics and Molecular Biology
Professor Sin-Hyeog Im's research lab focuses on the molecular and cellular mechanisms underlying autoimmune diseases, with a central emphasis on immune regulation, T cell differentiation, and the role of microbial and host factors in maintaining immune tolerance. The lab investigates how commensal microbiota, such as *Bifidobacterium bifidum*, influence regulatory T cell development and function, and explores key signaling pathways—like NFAT and HIF—involved in immune cell activation and tissue inflammation. Additionally, the lab develops antigen-specific immunotherapies, exemplified by oral tolerance induction using AChR fragments to treat autoimmune myasthenia gravis. Their work bridges innate and adaptive immunity, aiming to translate basic immunological insights into novel therapeutic strategies for chronic inflammatory and autoimmune disorders.
Figures are computed from collected data and may differ slightly.
Dysregulation of intestinal microflora is linked to inflammatory disorders associated with compromised immunosuppressive functions of Foxp3<sup>+</sup> T regulatory (T<sub>reg</sub>) cells. Although mucosa-associated commensal microbiota has been implicated in T<sub>reg</sub> generation, molecular identities of the "effector" components controlling this process remain largely unknown. Here, we have defined <i>Bifidobacterium bifidum</i> as a potent inducer of Foxp3<sup>+</sup> T<sub>reg</sub> ce
Ca2+/calcineurin-NFAT-mediated signaling pathways are involved in diverse cellular reactions by regulating gene expression either positively or negatively. The transcriptional activity of NFAT proteins can be either activating or deactivating depending on which binding partners are involved. Interaction of NFAT with AP-1 turns on the genes involved in active immune responses, while NFAT without cooperative binding of AP-1 turns on a T cell anergy program and blocks T cell activation and prolifer
The immunoregulatory cytokine interleukin 10 (IL-10) modulates the function of diverse immune and non-immune cells. Here, we examine the chromatin structural changes associated with IL10 gene transcription by naive and differentiated murine T cells. Naive T cells lack DNase I hypersensitive (HS) sites in the vicinity of the IL10 gene, whereas differentiated T cells display a strong 3' constitutive HS site as well as several inducible sites. The majority of HS sites map to regions that are strong
Myasthenia gravis (MG) and experimental autoimmune MG (EAMG) are T cell-dependent Ab-mediated autoimmune disorders, in which the nicotinic acetylcholine receptor (AChR) is the major autoantigen. Th1-type cells and costimulatory factors such as CD40 ligand (CD40L) contribute to disease pathogenesis by producing proinflammatory cytokines and by activating autoreactive B cells. In this study we demonstrate the capacity of CD40L blockade to modulate EAMG, and analyze the mechanism underlying this di
Rheumatoid arthritis (RA) is a systemic autoimmune disorder that manifests as chronic inflammation and joint tissue destruction. However, the etiology and pathogenesis of RA have not been fully elucidated. Here, we explored the role of the hypoxia-inducible factors (HIFs), HIF-1α (encoded by HIF1A) and HIF-2α (encoded by EPAS1). HIF-2α was markedly up-regulated in the intimal lining of RA synovium, whereas HIF-1α was detected in a few cells in the sublining and deep layer of RA synovium. Overexp
Myasthenia gravis (MG) is an autoimmune disorder in which the nicotinic acetylcholine receptor (AChR) is the major autoantigen. In an attempt to develop an antigen-specific therapy for MG, we administered a nonmyasthenogenic recombinant fragment of AChR orally to rats. This fragment, corresponding to the extracellular domain of the human AChR alpha-subunit (Halpha1-205), protected rats from subsequently induced experimental autoimmune myasthenia gravis (EAMG) and suppressed ongoing EAMG when tre
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