Hyun‐Ja Ko

ORCID: 0000-0002-9301-0704
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About
Contact & Profiles
Research Areas
  • Immunotherapy and Immune Responses
  • Immune Cell Function and Interaction
  • T-cell and B-cell Immunology
  • Immune Response and Inflammation
  • Cancer Research and Treatments
  • CAR-T cell therapy research
  • Inflammasome and immune disorders
  • RNA Interference and Gene Delivery
  • Diabetes and associated disorders
  • Virus-based gene therapy research
  • IL-33, ST2, and ILC Pathways
  • interferon and immune responses
  • Systemic Lupus Erythematosus Research
  • Heme Oxygenase-1 and Carbon Monoxide
  • Gut microbiota and health
  • Immune cells in cancer
  • Atherosclerosis and Cardiovascular Diseases
  • Retinoids in leukemia and cellular processes
  • Spondyloarthritis Studies and Treatments
  • Autoimmune and Inflammatory Disorders Research
  • Autophagy in Disease and Therapy
  • Pancreatic function and diabetes
  • Neutrophil, Myeloperoxidase and Oxidative Mechanisms
  • NF-κB Signaling Pathways
  • Viral Infectious Diseases and Gene Expression in Insects

Pohang University of Science and Technology
2019-2022

Institute for Basic Science
2019-2020

Walter and Eliza Hall Institute of Medical Research
2010-2015

The University of Melbourne
2014-2015

Monash University
2010-2011

Gain-of-function mutations that activate the innate immune system can cause systemic autoinflammatory diseases associated with increased IL-1β production. This cytokine is activated identically to IL-18 by an intracellular protein complex known as inflammasome; however, has not yet been specifically implicated in pathogenesis of hereditary disorders. We have now identified disease mice driven IL-18, but IL-1β, resulting from inactivating mutation actin-depolymerizing cofactor Wdr1....

10.1084/jem.20142384 article EN The Journal of Experimental Medicine 2015-05-25

Intracellular nucleotide binding and oligomerization domain (NOD) receptors recognize antigens including bacterial peptidoglycans initiate immune responses by triggering the production of pro-inflammatory cytokines through activating NF-κB MAP kinases. Receptor interacting protein kinase 2 (RIPK2) is critical for NOD-mediated activation cytokine production. Here we develop characterize a selective RIPK2 inhibitor, WEHI-345, which delays ubiquitylation downstream NOD engagement. Despite only...

10.1038/ncomms7442 article EN cc-by-nc-nd Nature Communications 2015-03-17

Abstract Although multiple dendritic cell (DC) subsets have the potential to induce Th17 differentiation in vitro, key DC that is critical induction and Th17-mediated disease remains moot. In this study, we revealed CCR2+ monocyte-derived DCs (moDCs), but not conventional DCs, were for vivo autoimmune inflammation. Functional comparison vitro indicated moDCs are most potent type of Th17-inducing compared with plasmacytoid DCs. Furthermore, demonstrated importance GM-CSF its endowment vivo,...

10.4049/jimmunol.1302040 article EN The Journal of Immunology 2014-02-01

Objective Interferon‐α (IFNα)–producing plasmacytoid dendritic cells (PDCs) are implicated in the pathogenesis of systemic lupus erythematosus (SLE). IFNα‐related genes highlighted among SLE susceptibility alleles and characteristically expressed blood patients with SLE, while mouse models lupus, PDC numbers IFNα production increased. This study was undertaken to investigate effects inhibitors that selectively target different antiapoptotic molecules on survival PDCs. Methods numbers, vitro...

10.1002/art.38966 article EN Arthritis & Rheumatology 2014-11-21

Food antigens drive spontaneous IgE elevation in the absence of microbiota by inducing IL-4–producing T follicular helper cells.

10.1126/sciadv.aaw1507 article EN cc-by-nc Science Advances 2019-05-03

Abstract Defects in the Bcl-2–regulated apoptotic pathway inhibit deletion of self-reactive T cells. What is unresolved, however, nature and fate such cells escaping deletion. In this study, we report that mice with defects contained increased numbers CD25lowFoxp3+ thymus peripheral lymph tissues. The population a large fraction bearing TCRs, evident from prominent increase self-superantigen–specific Foxp3+Vβ5+CD4+ BALB/c Bim−/− compared control animals. survival rate expanded was similar to...

10.4049/jimmunol.1100027 article EN The Journal of Immunology 2011-07-09

Migratory CD103+ and lymphoid-resident CD8+ dendritic cells (DCs) share many attributes, such as dependence on the same transcription factors, cross-presenting ability expression of certain surface molecules, that it has been proposed they belong to a common sub-lineage. The functional diversity two DC types is nevertheless incompletely understood. Here we reveal upon skin infection with herpes simplex virus, migratory DCs from draining lymph nodes were more potent at inducing Th17 cytokine...

10.1371/journal.pone.0091126 article EN cc-by PLoS ONE 2014-03-17

GM-CSF as an adjuvant has been shown to promote antitumor immunity in mice and humans; however, the underlying mechanism of GM-CSF-induced remains incompletely understood. In this study, we demonstrate that potentiates efficacy cancer vaccines through IL9-producing Th (Th9) cells. selectively enhanced Th9 cell differentiation by regulating COX2-PGE2 pathway while inhibiting induced regulatory T (iTreg) cells vitro vivo GM-CSF-activated monocyte-derived dendritic converted tumor-specific...

10.1158/2326-6066.cir-18-0518 article EN Cancer Immunology Research 2019-02-06

Abstract The autoimmune regulator (AIRE) promotes “promiscuous” expression of tissue‐restricted antigens (TRA) in thymic medullary epithelial cells to facilitate deletion autoreactive T‐cells. Here, we show that AIRE‐deficient mice showed an earlier development myelin oligonucleotide glycoprotein (MOG)‐induced experimental encephalomyelitis (EAE). To determine the outcome ectopic Aire expression, used a retroviral transduction system over‐express vitro , cell lines and bone marrow (BM). In...

10.1002/eji.201040679 article EN European Journal of Immunology 2010-09-21

CD8 + T cells are prominent in autoimmune diabetes of both humans and non‐obese diabetic (NOD) mice. For example, against islet‐specific glucose 6‐phosphatase catalytic subunit‐related protein (IGRP) can be detected readily older NOD It has been suggested that the enumeration peripheral blood may a predictive biomarker for type 1 (T1D). Here, we determined natural history functional endogenous IGRP 206–214 ‐specific cytotoxic lymphocytes (CTLs) mice with regard to age (3‐ 15‐week‐old...

10.1038/icb.2014.29 article EN Immunology and Cell Biology 2014-04-29

Haematopoietic stem cell (HSC) transfer coupled with gene therapy is a powerful approach to treating fatal diseases such as X-linked severe combined immunodeficiency. This ability isolate and genetically manipulate HSCs also offers strategy for inducing immune tolerance through ectopic expression of autoantigens. We have previously shown that retroviral transduction bone marrow (BM) vectors encoding the autoantigen, myelin oligodendrocyte glycoprotein (MOG), can prevent induction...

10.3109/08916934.2010.515274 article EN Autoimmunity 2010-10-01

Retinal dehydrogenase (RALDH) enzymatic activity catalyze the conversion of vitamin A to its metabolite Retinoic acid (RA) in intestinal dendritic cells (DCs) and promote immunological tolerance. However, precise understanding exogenous factors that act as initial trigger RALDH these is still evolving. By using germ-free (GF) mice raised on an antigen free (AF) elemental diet, we find certain components diet are critically required establish optimal expression activity, most prominently...

10.3389/fimmu.2020.01897 article EN cc-by Frontiers in Immunology 2020-08-11

Abstract Dietary antigens affect the adaptive immunity of host by inducing regulatory T cells and IgE-producing B cells. However, their roles in innate immune compartments such as lymphoid (ILCs) intestinal epithelial (IECs) are unclear. Here, using antigen-free (AF) mice, which germ-free (GF) mice fed with amino-acid-based diet, we found dietary proteins suppress development GATA-3-expressing ILC2s independent These produce more type 2 cytokines upregulated proliferation activation markers...

10.1038/s41598-022-11466-4 article EN cc-by Scientific Reports 2022-05-06

Autoinflammatory syndromes are caused by dysregulation of the innate immune system, frequently affecting inflammasome or other pathogen recognition pathways and leading to overproduction active IL-1 IL-18 (Masters et al., 2009).To date, there at least 12 known genetic causes autoinflammatory disease, including familial Mediterranean fever (FMF), hyper-IgD syndrome, cryopyrinassociated periodic syndrome.Therapeutic options for these diseases include nonsteroidal antiinflammatory drugs,...

10.1083/jcb.2095oia104 article EN The Journal of Cell Biology 2015-06-08

<div>Abstract<p>GM-CSF as an adjuvant has been shown to promote antitumor immunity in mice and humans; however, the underlying mechanism of GM-CSF–induced remains incompletely understood. In this study, we demonstrate that GM-CSF potentiates efficacy cancer vaccines through IL9-producing Th (Th9) cells. selectively enhanced Th9 cell differentiation by regulating COX2–PGE<sub>2</sub> pathway while inhibiting induced regulatory T (iTreg) cells <i>in...

10.1158/2326-6066.c.6550072 preprint EN 2023-04-04

<div>Abstract<p>GM-CSF as an adjuvant has been shown to promote antitumor immunity in mice and humans; however, the underlying mechanism of GM-CSF–induced remains incompletely understood. In this study, we demonstrate that GM-CSF potentiates efficacy cancer vaccines through IL9-producing Th (Th9) cells. selectively enhanced Th9 cell differentiation by regulating COX2–PGE<sub>2</sub> pathway while inhibiting induced regulatory T (iTreg) cells <i>in...

10.1158/2326-6066.c.6550072.v1 preprint EN 2023-04-04
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