Eun Young Choi

Yonsei University, Sŏul, Seoul, South Korea

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Publications (208)653.66 Total impact

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    ABSTRACT: To identify significant fluorescein angiographic (FA) characteristics associated with visual acuity (VA) in Behçet retinal vasculitis. Retrospective review of 86 eyes of 48 patients (age: 35.6±10.2 years) with Behçet retinal vasculitis were performed. VA and FA findings as well as correlation between them were assessed. The mean initial VA of eyes with posterior pole-involved vasculitis (63 eyes; 73.3%) was significantly worse than that of those with peripheral vasculitis (23 eye; 26.7%) (logarithm of the minimum angle of resolution VA: 0.554±0.572 vs. 0.078±0.148; p<0.0001). Subgroup analysis revealed a more severe and diffuse pattern of vascular leakage in posterior pole-involved vasculitis compared to peripheral vasculitis (p<0.0001). Retinal vascular leakage (β=0.345; p<0.0001), optic disc hyperfluorescence (β=0.147; p=0.032), and macular leakage (β=0.107; p=0.047) were significantly associated with worse initial VA. During the follow up (mean: 33.3±17.9 months), the change of leakage showed no significant correlation with change of VA in posterior pole-involved vasculitis (τ=0.199, p=0.092). Posterior pole involvement, the degree of retinal vascular leakage, optic disc hyperfluorescence, and macular leakage are significantly associated with VA in Behçet retinal vasculitis.
    Yonsei medical journal 07/2015; 56(4):1087-1096. DOI:10.3349/ymj.2015.56.4.1087 · 1.26 Impact Factor
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    ABSTRACT: Activation of IκB kinase (IKK) and NF-κB by genotoxic stresses modulates apoptotic responses and production of inflammatory mediators, thereby contributing to therapy resistance and premature aging. We previously reported that genotoxic agents induce nuclear localization of NEMO (NF-κB essential modulator) via an undefined mechanism to arbitrate subsequent DNA damage-dependent IKK/NF-κB signaling. Here we show that a nonclassical nuclear import pathway via IPO3 (importin 3, transportin 2) mediates stress-induced NEMO nuclear translocation. We found putative nuclear localization signals (NLS) in NEMO whose mutations disrupted stress-inducible nuclear translocation of NEMO and IKK/NF-κB activation in stably reconstituted NEMO-deficient cells. RNAi screening of both importin α and β family members, as well as co-immunoprecipitation analyses, revealed that a nonclassical importin β family member, IPO3, was the only importin that was able to associate with NEMO and whose reduced expression prevented genotoxic stress-induced NEMO nuclear translocation, IKK/NF-κB activation, and inflammatory cytokine transcription. Recombinant IPO3 interacted with recombinant NEMO but not NLS-mutant version and induced nuclear import of NEMO in digitonin-permeabilized cells. We also provide evidence that NEMO is disengaged from IKK complex following genotoxic stress induction. Thus, the IPO3 nuclear import pathway is an early and crucial determinant of the IKK/NF-κB signaling arm of the mammalian DNA damage response. Copyright © 2015, The American Society for Biochemistry and Molecular Biology.
    Journal of Biological Chemistry 06/2015; DOI:10.1074/jbc.M115.645960 · 4.60 Impact Factor
  • Jinkyeong Park, Eun Young Choi
    Journal of Parenteral and Enteral Nutrition 05/2015; 39(4):383-4. DOI:10.1177/0148607114556842 · 3.14 Impact Factor
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    ABSTRACT: Desmopressin is used for treating nocturnal polyuria, but hyponatremia is an associated concern in the elderly due to impaired urinary dilution. This study was undertaken to characterize hyponatremia occurring in adults using desmopressin for nocturnal polyuria. Data from 172 patients who were prescribed desmopressin for nocturnal polyuria at a urology clinic from September 2010 through February 2013 were retrospectively analyzed. Demographic and laboratory parameters were investigated to examine the risk factors for desmopressin-associated hyponatremia. The average follow-up serum sodium measured 21 ± 22 days after using desmopressin was 138 ± 5 mmol/l. Hyponatremia (<135 mmol/l) was found in 24 patients (14%), and it was severe in 7 (<126 mmol/l). In the hyponatremic patients, serum sodium decreased by 11 ± 6 mmol/l. Patients with hyponatremia were older than those with normonatremia (78 ± 7 vs. 68 ± 9 years, p < 0.0001). The presence of either hyponatremia-predisposing comorbidities or concurrent medications was associated with hyponatremia. Patients with hyponatremia had lower basal hemoglobin (11 ± 2 vs. 13 ± 2 g/dl, p < 0.001) and serum sodium (139 ± 2 vs. 140 ± 2 mmol/l, p < 0.05) than those with normonatremia. Multivariate logistic regression after adjustment for basal serum sodium showed that advanced age (OR 1.15; 95% CI 1.03-1.27) and lower hemoglobin level (OR 0.64; 95% CI 0.43-0.94) were independently associated with hyponatremia. Hyponatremia is not infrequently associated with desmopressin use. Those with advanced age (≥65 years) and lower hemoglobin are at risk of desmopressin-associated hyponatremia and need to be carefully monitored. © 2015 S. Karger AG, Basel.
    American Journal of Nephrology 04/2015; 41(3):183-190. DOI:10.1159/000381562 · 2.65 Impact Factor
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    ABSTRACT: Objectives The aim of this study was to evaluate HA coated with different ratios of TCP as a carrier for hABMSCs obtained during implant osteotomy in comparison to slowly-resorbing biomaterial, Bio-Oss, as a negative control, using in vitro and in vivo experiments.Materials and Methods Human ABMSCs (hABMSCs) harvested during implant osteotomy were transplanted using HA/TCP or Bio-Oss as carriers in a murine ectopic transplantation model (n = 12). Pore size and cell affinity were evaluated in vitro. The area of newly formed bone was analyzed histometrically, the number of osteocytes was counted, and immunohistochemical staining was conducted against several markers of osteogenesis, including alkaline phosphatase (ALP), runt-related transcription factor 2 (RUNX-2), osteocalcin (OCN), and osteopontin (OPN). Osteoclast formation was evaluated by tartrate-resistant acid phosphatase staining.ResultsThe carrier materials had comparable pore sizes. The cell affinity assay resulted in a high proportion of cell adhesion (>90%) in all experimental groups. Substantial new bone and osteocyte formation was observed on both HA/TCP carriers, whereas it was minimal with Bio-Oss. Positive immunostaining for ALP, RUNX-2, OCN, and OPN was observed with HA/TCP, but only limited expression of osteogenic markers with Bio-Oss. Conversely, there was a minimal osteoclast presence with Bio-Oss, but a significant presence of osteoclasts with both HA/TCP carriers.Conclusions Both types of scaffolds, BCP and Bio-Oss, showed high stem cell-carrying potential, but the in vivo healing patterns of their complexes with hABMSC could be affected by the microenvironment on the surfaces of the scaffolds. © 2015 Wiley Periodicals, Inc. J Biomed Mater Res Part B: Appl Biomater, 2015.
    Journal of Biomedical Materials Research Part B Applied Biomaterials 04/2015; DOI:10.1002/jbm.b.33416 · 2.33 Impact Factor
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    ABSTRACT: NF-κB essential modulator, NEMO, plays a key role in canonical NF-κB signaling induced by a variety of stimuli, including cytokines and genotoxic agents. To dissect the different biochemical and functional roles of NEMO in NF-κB signaling, various mutant forms of NEMO have been previously analyzed. However, transient or stable overexpression of wild-type NEMO can significantly inhibit NF-κB activation, thereby confounding the analysis of NEMO mutant phenotypes. What levels of NEMO overexpression lead to such an artifact and what levels are tolerated with no significant impact on NEMO function in NF-κB activation are currently unknown. Here we purified full-length recombinant human NEMO protein and used it as a standard to quantify the average number of NEMO molecules per cell in a 1.3E2 NEMO-deficient murine pre-B cell clone stably reconstituted with full-length human NEMO (C5). We determined that the C5 cell clone has an average of 4 x 105 molecules of NEMO per cell. Stable reconstitution of 1.3E2 cells with different numbers of NEMO molecules per cell has demonstrated that a 10-fold range of NEMO expression (0.6-6x105 molecules per cell) yields statistically equivalent NF-κB activation in response to the DNA damaging agent etoposide. Using the C5 cell line, we also quantified the number of NEMO molecules per cell in several commonly employed human cell lines. These results establish baseline numbers of endogenous NEMO per cell and highlight surprisingly normal functionality of NEMO in the DNA damage pathway over a wide range of expression levels that can provide a guideline for future NEMO reconstitution studies.
    PLoS ONE 03/2015; 10(3):e0116374. DOI:10.1371/journal.pone.0116374 · 3.53 Impact Factor
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    ABSTRACT: In allogeneic transplantation, including the B6 anti-BALB.B settings, H60 and H4 are two representative dominant minor histocompatibility antigens that induce strong CD8 T-cell responses. With different distribution patterns, H60 expression is restricted to hematopoietic cells, whereas H4 is ubiquitously expressed. H60-specific CD8 T-cell response has been known to be dominant in most cases of B6 anti-BALB.B allo-responses, except in the case of skin transplantation. To understand the mechanism underlying the subdominance of H60 during allogeneic skin transplantation, we investigated the dynamics of the H60-specific CD8 T cells in B6 mice transplanted with allogeneic BALB.B tail skin. Unexpectedly, longitudinal bioluminescence imaging and flow cytometric analyses revealed that H60-specific CD8 T cells were not always subdominant to H4-specific cells but instead showed a brief dominance before the H4 response became predominant. H60-specific CD8 T cells could expand in the draining lymph node and migrate to the BALB.B allografts, indicating their active participation in the anti-BALB.B allo-response. Enhancing the frequencies of H60-reactive CD8 T cells prior to skin transplantation reversed the immune hierarchy between H60 and H4. Additionally, H60 became predominant when antigen presentation was limited to the direct pathway. However, when antigen presentation was restricted to the indirect pathway, the expansion of H60-specific CD8 T cells was limited, whereas H4-specific CD8 T cells expanded significantly, suggesting that the temporary immunodominance and eventual subdominance of H60 could be due to their reliance on the direct antigen presentation pathway. These results enhance our understanding of the immunodominance phenomenon following allogeneic tissue transplantation.
    Experimental and Molecular Medicine 02/2015; 47(2). DOI:10.1038/emm.2014.107 · 2.46 Impact Factor
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    ABSTRACT: Background Individuals with panic disorder (PD) exhibit a hypersensitivity to inhaled carbon dioxide (CO2), possibly reflecting a lowered threshold for sensing signals of suffocation. Animal studies have shown that CO2-mediated fear behavior depends on chemosensing of acidosis in the amygdala via the acid sensing ion channel ASIC1a. We examined whether the human ortholog of the ASIC1a gene, ACCN2, is associated with the presence of PD and with amygdala structure and function. Methods We conducted a case-control analysis (N=414 PD cases, 846 healthy controls) of ACCN2single nucleotide polymorphisms (SNPs) and PD. We then tested whether variants showing significant association with PD are also associated with amygdala volume (n=1,048) and/or task-evoked reactivity to emotional stimuli (n=103) in healthy individuals. Results Two SNPs at the ACCN2 locus showed evidence of association with PD: rs685012 (OR=1.32, gene-wise corrected p=0.011) and rs10875995 (OR=1.26, gene-wise corrected p=0.046). The association appeared to be stronger when early-onset (age ≤ 20) PD cases and when cases with prominent respiratory symptoms were compared to controls. The PD risk allele at rs10875995 was associated with increased amygdala volume (p=0.035), as well as task-evoked amygdala reactivity to fearful and angry faces (p=0.0048). Conclusions Genetic variation at ACCN2 appears to be associated with PD and with amygdala phenotypes that have been linked to anxiety proneness. These results support the possibility that modulation of acid-sensing ion channels may have therapeutic potential for PD.
    Biological psychiatry 12/2014; DOI:10.1016/j.biopsych.2013.12.018 · 9.47 Impact Factor
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    ABSTRACT: Indoleamine 2,3-dioxygenases (IDOs) are tryptophan-catabolizing enzymes with immunomodulatory functions. However, the biological role of IDO2 and its relationship with IDO1 are unknown. To assess the relationship between IDO2 and IDO1, we investigated the effects of co-expression of human (h) IDO2 on hIDO1 activity. Cells co-expressing hIDO1 and hIDO2 showed reduced tryptophan metabolic activity compared with those expressing hIDO1 only. In a proteomic analysis, hIDO1-expressing cells exhibited enhanced expression of proteins related to the cell cycle and amino acid metabolism, and decreased expression of proteins related to cell survival. However, cells co-expressing hIDO1 and hIDO2 showed enhanced expression of negative regulators of cell apoptosis compared with those expressing hIDO1 only. Co-expression of hIDO1 and hIDO2 rescued the cell death induced by tryptophan-depletion through hIDO1 activity. Cells expressing only hIDO2 exhibited no marked differences in proteome profiles or cell growth compared with mock-transfectants. Cellular tryptophan metabolic activity and cell death were restored by co-expressing the hIDO2 mutant substituting the histidine 360 residue for alanine. These results demonstrate that hIDO2 plays a novel role as a negative regulator of hIDO1 by competing for heme-binding with hIDO1, and provide information useful for development of therapeutic strategies to control cancer and immunological disorders that target IDO molecules.
    Experimental and Molecular Medicine 11/2014; 46:e121. DOI:10.1038/emm.2014.69 · 2.46 Impact Factor
  • Cancer Research 10/2014; 74(19 Supplement):2084-2084. DOI:10.1158/1538-7445.AM2014-2084 · 9.28 Impact Factor
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    Korean Journal of Ophthalmology 10/2014; 28(5):424-426. DOI:10.3341/kjo.2014.28.5.424
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    ABSTRACT: Indoleamine 2,3-dioxygenase (IDO) is a rate-limiting enzyme in tryptophan catabolism that plays an important role in the induction of immune tolerance. Its role in graft-versus-tumor effect (GVT) after allogeneic stem cell transplantation (allo-SCT) remains unclear. Using a murine GVT model of reduced-intensity allo-HSCT followed by donor leukocyte infusion (DLI), we examined the role of IDO inhibition. Two stereoisomers of 1-methyl tryptophan (1-MT), a small-molecule inhibitor of IDO, reduced the growth of inoculated tumor in the mice that received DLI and had higher expression of IDO1 and IFNγ. However, L-1MT, but not D-1MT, mitigated tumor growth in mice that did not receive DLI and did not express IDO1 and IFNγ. Accordingly, both stereoisomers reduced plasma kynurenine concentrations early after DLI and enhanced in vitro cytotoxic lymphocyte function after allogeneic mixed lymphocyte reaction. Furthermore, L-1MT was more efficient in causing direct cytotoxic effects than D-1MT. Our results suggest that IDO inhibition can benefit in the setting of reduced-intensity allo-SCT using DLI.
    Experimental Hematology 10/2014; 42(10). DOI:10.1016/j.exphem.2014.06.006 · 2.81 Impact Factor
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    ABSTRACT: This study was carried out to know some regional gene difference in carabid beetle, Coptolabrus jankowskii. There are eight subspecies of this species in Korea and it was very difficult to identify by morphological similarity. The mitochondrial ND5 (NADH dehydrogenase subunit 5) gene of Coptolabrus jankowskii from four regions, Sangju, Daegu, Jumbongsan Mountain and Jejudo Island, was compared. The results showed the differences of the base sequence of total 57 sites and the amino acid variation of the 25 sites. The Neighbor-joining tree and Maximum parsimony tree were established based on sequence data of the ND5. In the NJ tree, the Jeju area except Songdangri, and Jumbongsan region showed close relationship group. In the case of Maximum parsimony tree, the result divided to three separated groups: the first connected group was Songdangri, Jeju area and the other the Korean peninsula regions except Jumbongsan. Others were Jeju area except Songdangri, and Jumbongsan region.
    09/2014; 7(4). DOI:10.1016/j.japb.2014.09.001
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    Jong Geol Jang, Kyung Soo Hong, Eun Young Choi
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    ABSTRACT: Hyaluronic acid is widely used in medical procedures, particularly in cosmetic procedures administered by physicians or nonmedical personnel. The materials used for cosmetic procedures by physicians as well as illegally by non-medical personnel can cause nonthrombotic pulmonary embolism (NTPE). We report the case of a woman with acute respiratory failure, neurologic symptoms and petechiae after an illegal procedure of hyaluronic acid dermal filler performed by an unlicensed medical practitioner 3 days before symptom onset. Although a few cases of NTPE after injection of hyaluronic acid have been reported yet, this is the first typical case showing a NTPE manifestation after the facial injection of hyaluronic acid.
    Tuberculosis and Respiratory Diseases 08/2014; 77(2):90-3. DOI:10.4046/trd.2014.77.2.90
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    Eun Young Choi, Dong-Ah Park, Jinkyeong Park
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    ABSTRACT: Background: The appropriate calorie intake to be provided to critically ill patients via enteral nutrition (EN) remains unclear. We performed a meta-analysis of randomized controlled trials to compare the effect of initial underfeeding and full feeding in acutely critically ill patients. Materials and Methods: We searched the Medline, EMBASE, and Cochrane Central Register of Controlled Trials databases to identify randomized controlled trials that compared underfeeding with full feeding in critically ill patients. The primary outcome was overall mortality. The secondary outcomes included length of hospital stay, length of intensive care unit (ICU) stay, duration of mechanical ventilation, incidence of pneumonia, Clostridium difficile colitis, other infectious complications, and gastrointestinal intolerance. Results: In total, 4 studies were included in this meta-analysis. There was no significant difference in overall mortality between the underfeeding and full-feeding groups (odds ratio [OR], 0.94; 95% confidence interval [CI], 0.74-1.19; I(2) = 26.6%; P = .61). Subgroup analysis of the underfeeding subgroup that was fed ≥33.3% of the standard caloric requirement indicated that overall mortality was significantly lower in this underfeeding subgroup than in the full-feeding group (OR, 0.63; 95% CI, 0.40-1.00; I(2) = 0%; P = .05). In contrast, no difference in overall mortality was noted between the underfeeding subgroup that was fed <33.3% of the standard caloric requirement and the full-feeding group. The length of hospital stay and length of ICU stay did not differ between the 2 groups. Moreover, no differences in other secondary clinical outcomes were noted. Conclusions: None of the analyzed clinical outcomes for the acutely critically ill patients were significantly influenced by the calorie intake of the initial EN.
    Journal of Parenteral and Enteral Nutrition 07/2014; 39(3). DOI:10.1177/0148607114544322 · 3.14 Impact Factor
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    Dataset: Jordan
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    ABSTRACT: Aim: We performed this study to evaluate the frequency of epidermal growth factor receptor (EGFR) mutations and their association with the histological subtype of lung adenocarcinoma diagnosed via small biopsy specimens. Patients and Methods: Three hundred and fifty-nine lung adenocarcinoma specimens were tested for EGFR mutation by a direct sequencing method. In 135 patients, histological subtypes were classified according to the 2011 International Association for the Study of Lung Cancer/American Thoracic Society/European Respiratory Society classification. We compared the EGFR mutation frequency by clinicopathological characteristics. Results: We detected 135 (37.6%) EGFR mutations and the incidence was highest in women who never smoked (54.6%). With regard to histological subtype, the highest prevalence of EGFR mutation was found in papillary (81.3%), followed by lepidic (70.4%), acinar (58.1%) and solid (28.3%) tumor types. In addition, the expression of thyroid transcription factor-1 was significantly higher in tumors with the EGFR mutation than in those without (p<0.001). Conclusion: The histological subtype of adenocarcinoma can be predictive of existing EGFR mutation, although the histology was confirmed using only small biopsies.
    Anticancer research 06/2014; 34(6):3189-3195. · 1.87 Impact Factor
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    ABSTRACT: Indoleamine 2,3-dioxygenase (IDO) is a rate-limiting enzyme for the tryptophan catabolism that plays an important role in the induction of immune tolerance. It is induced in the colon and exerts its effects there, regulating T-cell proliferation and survival. To address the role of IDO in acute graft-versus-host disease (AGVHD) after human allogeneic hematopoietic stem cell transplantation (allo-HSCT), we analyzed the relationship between IDO expression in colon tissues and clinical outcomes of 41 AGVHD patients who were diagnosed as gut AGVHD by a colon mucosal biopsy within 100 days posttransplantation. By in situ immunohistochemical analyses, IDO expression was measured in colon mucosal mononuclear cells (MNCs) and endothelial cells (ECs) in GVHD areas. High IDO expression in MNCs and low IDO expression in ECs had a trend toward a lower non-relapse mortality (NRM, p=0.157 and p=0.062, respectively). Multivariate analysis showed that combined high MNC + low EC IDO expression (p=0.046) and low disease risk (p=0.012) are associated with lower NRM. Paradoxical upregulation of IDO expression in colon MNCs and ECs may represent a new predictive factor for prognosis in gut AGVHD after human allo-HSCT.
    Experimental hematology 04/2014; 42(9). DOI:10.1016/j.exphem.2014.04.002 · 2.81 Impact Factor
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    ABSTRACT: Objective Several biomarkers reflecting inflammatory or proteolytic activity have been known to represent plaque vulnerability. Moreover, a recent study confirmed that contrast-enhanced ultrasound (CEUS) can visualize intraplaque neovascularization (IPN) and demonstrate plaque vulnerability. In this study, we tried to demonstrate that IPN detected by CEUS was correlated with several well-known biomarkers and clinical outcome in patients with coronary artery disease (CAD). Methods Patients with stable CAD were screened by conventional carotid ultrasound and patients with carotid plaque thickness more than 2 mm were performed by CEUS for the presence of IPN. Plasma levels of biomarkers and clinical outcomes were evaluated. Results Among consecutive 89 patients fulfilled the inclusion criteria, 30 patients without IPN (group 1) and 59 patients with IPN (group 2) were analyzed. There were no significant difference in baseline characteristics except for mean age (62.9 ± 10.1 yrs versus 68.4 ± 9.6 yrs, p = 0.015). On multivariate analysis, only MMP-9 (p = 0.021, 95% CI 1.002–1.027) showed a significant association with IPN. But patients with IPN showed only trend for a history of cardiovascular disease (CVD) (44% versus 30%, p = 0.19) and one-year cardiovascular events (CVE) (6.8% versus 3.3%, p = 0.50) compared to group 1. Maximum plaque thickness (p = 0.04, 95% CI 1.230–6.322) showed a significant correlation with the clinical outcome including CVD or CVE. Conclusion MMP-9 correlated with IPN on CEUS. For clinical implication, however, large prospective studies are needed.
    Atherosclerosis 04/2014; 233(2):579–583. DOI:10.1016/j.atherosclerosis.2014.01.042 · 3.97 Impact Factor
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    ABSTRACT: Graft-versus-host disease (GVHD) is a fatal complication that occurs after allogeneic hematopoietic stem cell transplantation. To understand the dynamics of CD4 and CD8 T cell production of IFN-γ and IL-17 during GVHD progression, we established a GVHD model by transplanting T cell-depleted bone marrow (TCD-BM) and purified T cells from B6 mice into irradiated BALB.B, creating an MHC-matched but minor histocompatibility (H) antigen-mismatched transplantation (B6 → BALB.B GVHD). Transplantation-induced GVHD was confirmed by the presence of the appropriate compositional changes in the T cell compartments and innate immune cells in the blood and the systemic secretion of inflammatory cytokines. Using this B6 → BALB.B GVHD model, we showed that the production of IFN-γ and IL-17 by CD4 T cells preceded that by CD8 T cells in the spleen, mesenteric lymph node, liver, and lung in the BALB.B GVHD host, and Th1 differentiation predated Th17 differentiation in all organs during GVHD progression. Such changes in cytokine production were based on changes in cytokine gene expression by the T cells at different time points during GVHD development. These results demonstrate that both IFN-γ and IL-17 are produced by CD4 and CD8 T cells but with different kinetics during GVHD progression.
    Immune Network 04/2014; 14(2):89-99. DOI:10.4110/in.2014.14.2.89

Publication Stats

2k Citations
653.66 Total Impact Points

Institutions

  • 2015
    • Yonsei University
      • College of Dentistry
      Sŏul, Seoul, South Korea
    • University of Wisconsin–Madison
      Madison, Wisconsin, United States
  • 2014–2015
    • Yonsei University Hospital
      • Department of Internal Medicine
      Sŏul, Seoul, South Korea
    • Kyung Hee University
      Sŏul, Seoul, South Korea
  • 2013–2015
    • Hanyang University Medical Center
      Sŏul, Seoul, South Korea
    • Asan Medical Center
      Sŏul, Seoul, South Korea
    • Ewha Womans University
      • Department of Physics
      Sŏul, Seoul, South Korea
  • 2013–2014
    • Seoul National University Bundang Hospital
      • Department of Pediatrics
      Sŏul, Seoul, South Korea
  • 2012–2014
    • Harvard University
      • Department of Psychology
      Cambridge, Massachusetts, United States
    • Ulsan University Hospital
      Urusan, Ulsan, South Korea
    • Dankook University
      Eidō, North Chungcheong, South Korea
    • Korea Internet & Security Agency
      Sŏul, Seoul, South Korea
  • 2009–2014
    • Kyungpook National University
      • • College of Ecology and Environmental Science
      • • Applied Biology
      • • School of Life Science
      Daikyū, Daegu, South Korea
    • National Health Insurance Corporation Ilsan Hospital
      Sŏul, Seoul, South Korea
    • National Institutes of Health
      • Branch of Experimental Immunology
      Maryland, United States
    • Northern Inyo Hospital
      BIH, California, United States
  • 2004–2014
    • Yeungnam University
      • • Division of Internal Medicine
      • • College of Medicine
      Gyeongsan, Gyeongsangbuk-do, South Korea
  • 1997–2014
    • Seoul National University Hospital
      • • Department of Internal Medicine
      • • Department of Thoracic and Cardiovascular Surgery
      • • Department of Nuclear Medicine
      • • Department of Pathology
      Sŏul, Seoul, South Korea
  • 1996–2014
    • Seoul National University
      • • Department of Biomedical Sciences
      • • Department of Pediatrics
      • • Department of Pathology
      • • College of Pharmacy
      Sŏul, Seoul, South Korea
    • Chungbuk National University
      Chinsen, Chungcheongbuk-do, South Korea
  • 2010–2013
    • Sejong General Hospital
      Bucheon, Gyeonggi-do, South Korea
  • 2011–2012
    • University of Ulsan
      • Graduate School
      Urusan, Ulsan, South Korea
    • National Cancer Center Korea
      • Specific Organs Cancer Branch
      Kōyō, Gyeonggi Province, South Korea
    • Kwandong University
      Gangneung, Gangwon, South Korea
    • Ajou University
      Sŏul, Seoul, South Korea
    • Korea Institute of Science and Technology
      Sŏul, Seoul, South Korea
  • 2010–2012
    • Hongik University
      • Department of Chemical Engineering
      Sŏul, Seoul, South Korea
  • 2010–2011
    • Seegene Institute of Life Sciences
      Sŏul, Seoul, South Korea
  • 2008–2011
    • National Cancer Institute (USA)
      • Experimental Immunology Branch
      Maryland, United States
  • 2000–2010
    • Pusan National University
      • • Department of Chemistry
      • • Division of Materials Science and Engineering
      Tsau-liang-hai, Busan, South Korea
  • 2007–2009
    • NCI-Frederick
      Фредерик, Maryland, United States
  • 2006–2007
    • Korea University
      • Department of Life Sciences
      Sŏul, Seoul, South Korea
    • Dankook University Hospital
      Anjŏ, Gyeonggi Province, South Korea
  • 2005–2006
    • Inha University
      • College of Medicine
      Sŏul, Seoul, South Korea
  • 2004–2005
    • Sungkyunkwan University
      • • Department of Chemistry
      • • Institute of Basic Science
      Sŏul, Seoul, South Korea
  • 2003
    • The Jackson Laboratory
      Bar Harbor, Maine, United States
    • Wonkwang University School of Medicine and Hospital
      Riri, North Jeolla, South Korea
    • Blood Systems Research Institute
      San Francisco, California, United States
  • 1999
    • Inje University Paik Hospital
      Sŏul, Seoul, South Korea