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Search Results: 1 - 10 of 25692 matches for " Ho-Youn Kim "
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Traditional Knowledge and ex situ Conservation of Some Threatened Medicinal Plants of Swat Kohistan, Pakistan
Muhammad Hamayun,Sumera Afzal Khan,Ho-Youn Kim,Chae In Na
International Journal of Botany , 2006,
Abstract: Medicinal plants still provide primary health care to human race in different regions across the globe, especially in the developing world. The role of medicinal herbs as source of traditional medicine have decreased due to the introduction of allopathic drugs but still their importance as a prime source of rural health care can not be paralleled. Medicinal plants and their pertinent knowledge need to be conserved for the future generations. During present study, traditional knowledge of 16 threatened medicinal plants of Swat Kohistan was documented and a nursery was raised in lower Swat in an effort to conserve them. Only 8 plant species viz. Bergenia ciliata, Dioscorea deltoidea, Bistorta amplexicaulis, Valeriana jatamansi, Valeriana pyrolifolia, Viola biflora, Viola canescens and Berberis lycium survived and acclimatized to new habitat, while the rest failed to germinate.
IL-17 induces production of IL-6 and IL-8 in rheumatoid arthritis synovial fibroblasts via NF-κB- and PI3-kinase/Akt-dependent pathways
Sue-Yun Hwang, Ju-Young Kim, Kyoung-Woon Kim, Mi-Kyung Park, Youngmee Moon, Wan-Uk Kim, Ho-Youn Kim
Arthritis Research & Therapy , 2004, DOI: 10.1186/ar1038
Abstract: Increasing attention is being given to the role of IL-17, a proinflammatory cytokine produced by activated T cells, in the perpetuation of joint inflammation in rheumatoid arthritis (RA) [1-3]. Overproduction of this cytokine has been associated with elevated production of proinflammatory mediators such as IL-6, IL-8, granulocyte/macrophage-colony-stimulating factor, GRO-α, and prostaglandin E2 in various cell types [4,5]. Of these targets, IL-6 and IL-8 are most likely to act as major instigators of RA joint inflammation, since disruption of their functions either by gene knockout [6] or by systemic IL-4 treatment [7] leads to protection against arthritis in animal models. Early studies have also denominated IL-1β and tumor necrosis factor α (TNF-α) as major inducers of IL-6 and IL-8 in RA synovium, and IL-17 appears to exert an additive and synergistic effect with these two cytokines [5]. However, results from studies using mice and human joint explants suggest that IL-17 is capable of provoking inflammatory responses by itself [8,9]. Yet by comparison with the vast information about the role of IL-1β and TNF-α in synovial inflammation, relatively little is known about the mode of IL-17-mediated activation.The cytoplasmic tail of IL-17R (IL-17 receptor) does not contain any known motifs associated with intracellular signaling, and not much is known about the pathway that relays IL-17-mediated stimulation on to the induction of target cytokines. The involvement of JAK/STAT (Janus kinase/signal transducer and activator of transcription) and TRAF6 (TNF-receptor-associated factor 6) has been suggested to transmit IL-17 signaling in human monocyte cell line [10] and embryonic fibroblasts [11], respectively, and yet cytoplasmic players transmitting IL-17-mediated activation in RA synovial fibroblasts remain to be investigated. Moreover, recent searches using the characteristic 'four-cysteine motif' of IL-17 identified a panoply of IL-17 family members, listed as IL-17B
Increased interleukin-17 production via a phosphoinositide 3-kinase/Akt and nuclear factor κB-dependent pathway in patients with rheumatoid arthritis
Kyoung-Woon Kim, Mi-La Cho, Mi-Kyung Park, Chong-Hyeon Yoon, Sung-Hwan Park, Sang-Heon Lee, Ho-Youn Kim
Arthritis Research & Therapy , 2004, DOI: 10.1186/ar1470
Abstract: Rheumatoid arthritis (RA) is characterized by infiltrations of macrophages and T cells into the joint, and synovial hyperplasia. Proinflammatory cytokines released from these cells are known to be important in the destruction of joints in RA [1]. The favorable clinical benefits obtained with inhibitors of tumor necrosis factor (TNF)-α) and interleukin (IL)-1 suggest that the blockade of key inflammatory cytokines has been the important issue in the development of new therapeutic applications [2].A little over a decade ago, the primacy of T cells in the pathogenesis of autoimmune disease such as RA was undisputed because they are the largest cell population infiltrating the synovium. However, a series of studies demonstrated paucity of T cell-derived cytokines such as IL-2 and interferon-γ in the joints of RA, whereas macrophage and fibroblast cytokines including IL-1, IL-6, IL-15, IL-18 and TNF-α were abundant in rheumatoid synovium. This paradox has questioned the role of T cells in the pathogenesis of RA [3]. Because we have already demonstrated the enhanced proliferation of antigen specific T cells, especially to type II collagen, and the skewing of T helper type 1 (Th1) cytokines in RA [4], the role of T cells needs to be elucidated in different aspects.IL-17 is one of the inflammatory cytokines secreted mainly by activated T cells, which can induce IL-6 and IL-8 by fibroblasts [5]. This cytokine is of interest for two major reasons: first, similarly to TNF-α and IL-1, IL-17 has proinflammatory properties; second, it is produced by T cells [6]. Recent observations demonstrated that IL-17 can also activate osteoclastic bone resorption by the induction of RANKL (receptor activator of nuclear factor κB [NF-κB] ligand), which is involved in bony erosion in RA [7]. It also stimulates the production of IL-6 and leukemia inhibitory factor by synoviocytes, and of prostaglandin E2 and nitric oxide by chondrocytes, and has the ability to differentiate and activate the den
Dysfunctional interferon-α production by peripheral plasmacytoid dendritic cells upon Toll-like receptor-9 stimulation in patients with systemic lupus erythematosus
Seung-Ki Kwok, June-Yong Lee, Se-Ho Park, Mi-La Cho, So-Youn Min, Sung-Hwan Park, Ho-Youn Kim, Young-Gyu Cho
Arthritis Research & Therapy , 2008, DOI: 10.1186/ar2382
Abstract: The concentrations of IFN-α were determined in serum and culture supernatant of peripheral blood mononuclear cells (PBMCs) from SLE patients and healthy controls after stimulation with CpG ODN2216 or SLE serum. The numbers of circulating pDCs were analyzed by fluoresence-activated cell sorting analysis. pDCs were treated with CpG ODN2216 and SLE serum repeatedly, and levels of produced IFN-α were measured. The expression of IFN-α signature genes and inhibitory molecules of TLR signaling were examined in PBMCs from SLE patients and healthy control individuals.Although there was no significant difference in serum concentration of IFN-α and number of circulating pDCs between SLE patients and healthy control individuals, the IFN-α producing capacity of PBMCs was significantly reduced in SLE patients. Interestingly, the degree which TLR9 ligand-induced IFN-α production in SLE PBMCs was inversely correlated with the SLE serum-induced production of IFN-α in healthy PMBCs. Because repeated stimulation pDCs with TLR9 ligands showed decreased level of IFN-α production, continuous TLR9 stimulation may lead to decreased production of IFN-α in SLE PBMCs. In addition, PBMCs isolated from SLE patients exhibited higher expression of IFN-α signature genes and inhibitory molecules of TLR signaling, indicating that these cells had already undergone IFN-α stimulation and had become desensitized to TLR signaling.We suggest that the persistent presence of endogenous IFN-α inducing factors induces TLR tolerance in pDCs of SLE patients, leading to impaired production of IFN-α.Systemic lupus erythematosus (SLE) is a systemic autoimmune disease that is characterized by generation of autoantibodies against nuclear DNA and/or nuclear proteins [1]. The precise pathogenesis of SLE remains unknown, but both genetic and environmental factors are involved [2]. Over the past two decades numerous studies have suggested that interferon (IFN)-α may play a pathogenic role in SLE. This view is derived fr
Impact of interleukin-21 in the pathogenesis of primary Sjogren's syndrome: increased serum levels of interleukin-21 and its expression in the labial salivary glands
Kwi Kang, Hyun-Ok Kim, Seung-Ki Kwok, Ji Ju, Kyung-Su Park, Dong-Il Sun, Joo Jhun, Hye Oh, Sung-Hwan Park, Ho-Youn Kim
Arthritis Research & Therapy , 2011, DOI: 10.1186/ar3504
Abstract: Serum IL-21 levels in 40 primary SS, 40 rheumatoid arthritis (RA), and 38 systemic lupus erythematosus (SLE) patients and 20 healthy controls were measured. Serum IL-21 levels of SS patients were assessed for correlations with laboratory data, including anti-nuclear antibody, anti-Ro/La antibodies, globulin, immunoglobulin (Ig) class, and IgG subclass. LSGs from 16 primary SS and 4 controls with sicca symptoms were evaluated for IL-21 and IL-21 receptor (IL-21R) expression by immunohistochemistry. Confocal microscopy was performed to further characterize the IL-21 positive cells.Primary SS patients had significantly higher serum IL-21 levels than controls, and these increments correlated positively with levels of IgG, IgG1. Serum IgG1 levels correlated with anti-Ro antibody titers. Immunohistochemical analyses showed that lymphocytic foci and the periductal area of the LSGs from SS patients expressed high levels of IL-21 and lower levels of IL-21R, whereas the control LSGs showed minimal expression of both antigens. The more the lymphocyte infiltrated, IL-21expression in LSGs showed a tendency to increase. Confocal microscopic analyses revealed that IL-21 expressing infiltrating lymphocytes in the LSGs of SS patients also expressed CXCR5.Primary SS is associated with high serum IL-21 levels that correlate positively with serum IgG, especially IgG1, levels. The expression of IL-21 is increased as more lymphocytes infiltrated in LSGs. These observations suggest that IL-21 may play an important role in primary SS pathogenesis.IL-21 is a pleiotropic cytokine that belongs to the common cytokine receptor γ chain (γc)-dependent cytokine family, which is produced by activated CD4+ T cells and NKT cells [1]. The IL-21 receptor (IL-21R) consists of the IL-21R α chain and the γc chain and is expressed on T cells, NK cells, NKT cells, B cells, dendritic cells (DCs) and macrophages as well as on non-hematopoietic cells, including keratinocytes and fibroblasts [2]. The activation
Patients with systemic lupus erythematosus have abnormally elevated Epstein–Barr virus load in blood
Uk Moon, Su Park, Sang Oh, Wan-Uk Kim, Sung-Hwan Park, Sang-Heon Lee, Chul-Soo Cho, Ho-Youn Kim, Won-Keun Lee, Suk Lee
Arthritis Research & Therapy , 2004, DOI: 10.1186/ar1181
Abstract: Systemic lupus erythematosus (SLE) is an idiopathic disease characterized by variable inflammatory destruction. A variety of autoantibodies are found in the serum of SLE patients, indicating that SLE is an autoimmune disease [1]. However, the mechanisms that lead to the aberrant autoimmune responses are not clearly understood, and various genetic and environmental factors are thought to be involved [2]. Epstein–Barr virus (EBV) is suspected to play a role in predisposing to SLE for several reasons. First, EBV promotes proliferation of B cells after infection, and thus it poses a prolonged antigenic challenge. This prolonged EBV antigen expression may trigger SLE in genetically prone individuals. Second, EBV-infected B cells can become a continuous source of autoantibodies. Third, sequence homologies exist between SLE autoantigens and some EBV proteins, such as EBV nuclear antigen (EBNA)-1 and EBNA-2. The antibodies elicited by these viral antigens may cross-react with autoantigens and trigger SLE [3-5].If EBV is indeed involved in the pathogenesis of SLE, then there must be some association between EBV infection and SLE [6-9]. Elevated titers of anti-EBV antibodies have been detected in SLE patients compared with control individuals [10-12]. It is difficult to prove that there is any association between EBV and SLE by comparing seroconversion rates between patients and healthy control individuals because the majority of adults are seropositive for EBV [13]. Recently, James and coworkers [14,15] examined more than 100 SLE patients and found that the EBV seroconversion rate was significantly greater in SLE patients than in normal control individuals, both in young and adult populations. However, these studies do not prove the existence of a temporal relationship between EBV infection and development of SLE. In addition, measuring antibodies to EBV antigen does not directly indicate the status of EBV within the body. This is because the serologic response can be affect
TLR2 ligation induces the production of IL-23/IL-17 via IL-6, STAT3 and NF-kB pathway in patients with primary Sjogren's syndrome
Seung-Ki Kwok, Mi-La Cho, Yang-Mi Her, Hye-Joa Oh, Mi-Kyung Park, Seon-Yeong Lee, Yun Woo, Ji Ju, Kyung-Su Park, Ho-Youn Kim, Sung-Hwan Park
Arthritis Research & Therapy , 2012, DOI: 10.1186/ar3780
Abstract: The expressions of various TLRs, IL-17 and the cytokines involved in Th17 cell differentiation including IL-6, IL-23, tumor necrosis factor-alpha (TNF-α) and IL-1β were examined by immunohistochemistry in salivary glands of pSS patients. The IL-17 producing CD4+ T cells (Th17 cells) were examined by flow cytometry and confocal staining in peripheral mononuclear blood cells (PMBCs) and salivary glands of pSS patients. After PBMCs were treated with TLR specific ligands, the induction of IL-17 and IL-23 was determined using real-time PCR and ELISA. The signaling pathway that mediates the TLR2 stimulated production of IL-17 and IL-23 was investigated by using treatment with specific signaling inhibitors.We showed that TLR2, TLR4, TLR6, IL-17 and the cytokines associated with Th17 cells were highly expressed in salivary glands of pSS patients but not in controls. The expressions of TLR2, TLR4 and TLR6 were observed in the infiltrating mononuclear cells and ductal epithelial cells, whereas IL-17 was mainly observed in infiltrating CD4+ T cells. The number of IL-17 producing CD4+ T cells was significantly higher in pSS patients both in PBMCs and minor salivary glands. The stimulation of TLR2, TLR4 and TLR6 additively induced the production of IL-17 and IL-23 from the PBMCs of pSS patients especially in the presence of TLR2 stimulation. IL-6, signal transducer and activator of transcription 3 (STAT3) and nuclear factor-kappaB (NF-kB) pathways were implicated in the TLR2 stimulated IL-17 and IL-23.Our data demonstrate that TLR2 ligation induces the production of IL-23/IL-17 via IL-6, STAT3 and NF-kB pathway in pSS. Therefore, therapeutic strategies that target TLR/IL-17 pathway might be strong candidates for treatment modalities of pSS.Sj?gren's syndrome (SS) is a relatively common autoimmune exocrinopathy that is associated with infiltration of lymphocytes and is characterized by gradually progressive lachrymal and salivary dysfunction [1,2]. The exocrine dysfunction can oc
Curcumin Attenuates Acute Graft-versus-Host Disease Severity via In Vivo Regulations on Th1, Th17 and Regulatory T Cells
Min-Jung Park, Su-Jin Moon, Sung-Hee Lee, Eun-Ji Yang, Jun-Ki Min, Seok-Goo Cho, Chul-Woo Yang, Sung-Hwan Park, Ho-Youn Kim, Mi-La Cho
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0067171
Abstract: Background In this study we examined the in vivo and in vitro effects and mechanisms of action of curcumin on the development of acute graft-versus-host disease (GVHD) using a murine model. Methodology/Principal Findings Mixed lymphocyte reactions were used to determine the in vitro effects of curcumin. Treatment with curcumin attenuated alloreactive T cell proliferation and inhibited the production of interferon (IFN)-γ and interleukin (IL)-17. In a murine acute GVHD model, transplantation of curcumin-treated allogeneic splenocytes into irradiated recipient mice significantly reduced the clinical severity scores of acute GVHD manifested in the liver, skin, colon and lung as compared with animals receiving vehicle-treated splenocytes. c-Fos and c-Jun expression levels in the skin and intestine, which are major target organs, were analyzed using immunohistochemical staining. Expression of both proteins was reduced in epithelial tissues of skin and intestine from curcumin-treated GVHD animals. The IFN-γ-expressing CD4+ splenocytes and IFN-γ-expressing lymph node cells were dramatically decreased in curcumin-treated mice. In contrast, CD4+Foxp3+ splenocytes were increased in the curcumin-treated acute GVHD animals. Flow cytometric analysis revealed that animals transplanted with curcumin-treated allogeneic splenocytes showed increased populations of CD4+ regulatory T cells (Tregs) as well as CD8+ Treg cells, compared to animals administered vehicle-treated splenocytes. Curcumin-treated acute GVHD animals could have a change in B cell subpopulations. Conclusion/Significance In the present study, we investigated the efficacy and mechanism of action of curcumin treatment against acute GVHD. The acute GVHD mice administered with curcumin-treated splenocytes showed significantly reduced severity of acute GVHD. Curcumin exerted in vivo preventive effects on acute GVHD by reciprocal regulation of T helper 1 (Th1) and Treg (both CD4+ and CD8+ Treg) cell lineages as well as B cell homeostasis.
Induction of IL-10-producing CD4+CD25+ T cells in animal model of collagen-induced arthritis by oral administration of type II collagen
So-Youn Min, Sue-Yun Hwang, Kyung-Su Park, Jae-sun Lee, Kang-Eun Lee, Kyung-Wun Kim, Young-Ok Jung, Hyunk-Jae Koh, Ju-Ho Do, Haerim Kim, Ho-Youn Kim
Arthritis Research & Therapy , 2004, DOI: 10.1186/ar1169
Abstract: Oral tolerance is a state of absent or minimal immune responsiveness to protein antigens that were repeatedly administered by oral feeding [1]. Induction of peripheral tolerance by oral administration of antigen has been applied to the treatment of autoimmune diseases such as rheumatoid arthritis (RA) [2,3], multiple sclerosis, systemic sclerosis, type I diabetes and iritis [4], but the mechanisms by which orally administered antigen can induce peripheral tolerance have not yet been elucidated. Studies conducted in animal models have suggested that the possible mechanism may involve secretion of anti-inflammatory cytokines including IL-4, IL-10 and transforming growth factor (TGF)-β by mucosal T lymphocytes that have differentiated into T-helper (Th)2 or Th3 cells after encountering the antigen [5-7]. However, individual studies often report conflicting findings, depending on the route, dose and timing of antigen administration [8].Although much of the RA pathogenesis remains to be elucidated, it has been reported that joint proteins, probably type II collagen (CII), play a key role in the instigation of T-cell mediated immune responses. Administration of CII to DBA/1 mice induces polyarthritis with pathological symptoms similar to those observed in human RA [9,10]. In order to investigate the cellular mechanisms that underlie oral tolerance, we studied an animal model of collagen-induced arthritis (CIA), in which mice undergo repeated oral administration of CII, and monitored changes in immune cell function and factors associated with inflammation. We found that serum levels of IgG subtypes, as well as the production of IL-10, TGF-β and IFN-γ, were affected in tolerized mice. We also noticed greater proportions of IL-10-producing CD4+CD25+ T cells in the Peyer's patch, mesenteric lymph nodes and the spleen of tolerized mice. Production of these cells, exhibiting the characteristics of the Treg subset, was induced to a significant degree by lymphocytes from tolerize
Indoleamine 2,3-dioxygenase-expressing dendritic cells are involved in the generation of CD4+CD25+ regulatory T cells in Peyer's patches in an orally tolerized, collagen-induced arthritis mouse model
Min-Jung Park, So-Youn Min, Kyung-Su Park, Young-Gyu Cho, Mi-La Cho, Young-Ok Jung, Hyun-Sil Park, Soog-Hee Chang, Seok Cho, Jun-Ki Min, Sung-Hwan Park, Ho-Youn Kim
Arthritis Research & Therapy , 2008, DOI: 10.1186/ar2361
Abstract: Type II collagen was fed six times to DBA/1 mice beginning 2 weeks before immunization, and the effect on arthritis was assessed. To examine the IDO expression, the DCs of messenger RNA and protein were analyzed by RT-PCR and Flow cytometry. In addition, a proliferative response assay was also carried out to determine the suppressive effects of DCs through IDO. The ability of DCs expressing IDO to induce CD4+CD25+ T regulatory cells was examined.CD11c+ DCs in Peyer's patches from orally tolerized mice expressed a higher level of IDO than DCs from nontolerized CIA mice. IDO-expressing CD11c+ DCs were involved in the suppression of type II collagen-specific T-cell proliferation and in the downregulation of proinflammatory T helper 1 cytokine production. The suppressive effect of IDO-expressing CD11c+ DCs was mediated by Foxp3+CD4+CD25+ regulatory T cells.Our data suggest that tolerogenic CD11c+ DCs are closely linked with the induction of oral tolerance through an IDO-dependent mechanism and that this pathway may provide a new therapeutic modality to treat autoimmune arthritis.Repeated oral administration of autoantigen can suppress autoimmune responses in collagen-induced arthritis (CIA) and experimental autoimmune encephalomyelitis, and can suppress diabetes in nonobese diabetic mice [1-10]. Although the mechanisms responsible for the induction of oral tolerance have not been elucidated fully, repeated oral administration of a high dose of antigen can induce oral tolerance by anergy or deletion of antigen-specific T cells. In contrast, repeated feeding of a low dose of antigen favors the induction of active immune regulation involving regulatory T cells, including transforming growth factor beta (TGFβ)-producing T helper 3 cells, IL-10-producing T regulatory 1 cells, and CD4+CD25+ T cells [1,10,11]. Previous studies have demonstrated that, after repeated oral administration of type II collagen (CII) and subsequent induction of CIA, the mean arthritis index is lower
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