• Title/Summary/Keyword: cell infection

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Experimental Study on Inhibition Effects of the XAF1 Gene against Lung Cancer Cell Proliferation

  • Yang, Wen-Tao;Chen, Dong-Lai;Zhang, Fu-Quan;Xia, Ying-Chen;Zhu, Rong-Ying;Zhou, Duan-Shan;Chen, Yong-Bing
    • Asian Pacific Journal of Cancer Prevention
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    • v.15 no.18
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    • pp.7825-7829
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    • 2014
  • Objective: To investigate the effect of high expression of XAF1 in vivo or in vitro on lung cancer cell growth and apoptosis. Methods: 1. The A549 human lung cancer cell line was transfected with Ad5/F35 - XAF1, or Ad5/F35 - Null at the same multiplicity of infection (MOI); (hereinafter referred to as transient transfected cell strain); XAF1 gene mRNA and protein expression was detected by reverse transcription polymerase chain reaction (RT-PCR) and Western blotting respectively. 2. Methyl thiazolyl tetrazolium (MTT) and annexin V-FITC/PI double staining were used to detect cell proliferation and apoptosis before and after infection of Ad5/F35 - XAF1 with Western blotting for apoptosis related proteins, caspase 3, caspase - 8 and PARP. 3. After the XAF1 gene was transfected into lung cancer A549 cells by lentiviral vectors, and selected by screening with Blasticidin, reverse transcription polymerase chain reaction (RT-PCR) and Western blotting were applied to detect mRNA and protein expression, to establish a line with a stable high expression of XAF1 (hereinafter referred to as stable expression cell strain). Twenty nude mice were randomly divided into groups A and B, 10 in each group: A549/XAF1 stable expression cell strain was subcutaneously injected in group A, and A549/Ctrl stable cell line stable expression cell strain in group B (control group), to observe transplanted tumor growth in nude mice. Results: The mRNA and protein expression of XAF1 in A549 cells transfected by Ad5/F35 - XAF1 was significantly higher than in the control group. XAF1 mediated by adenovirus vector demonstrated a dose dependent inhibition of lung cancer cell proliferation and induction of apoptosis. This was accompanied by cleavage of caspase -3, -8, -9 and PARP, suggesting activation of intrinsic or extrinsic apoptotic pathways. A cell strain of lung cancer highly expressing XAF1 was established, and this demonstrated delayed tumor growth after transplantation in vivo. Conclusion: Adenovirus mediated XAF1 gene expression could inhibit proliferation and induce apoptosis in lung cancer cells in vitro; highly stable expression of XAF1 could also significantly inhibit the growth of transplanted tumors in nude mouse, with no obvious adverse reactions observed. Therefore, the XAF1 gene could become a new target for lung cancer treatment.

Signaling for Synergistic Activation of Natural Killer Cells

  • Kwon, Hyung-Joon;Kim, Hun Sik
    • IMMUNE NETWORK
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    • v.12 no.6
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    • pp.240-246
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    • 2012
  • Natural killer (NK) cells play a pivotal role in early surveillance against virus infection and cellular transformation, and are also implicated in the control of inflammatory response through their effector functions of direct lysis of target cells and cytokine secretion. NK cell activation toward target cell is determined by the net balance of signals transmitted from diverse activating and inhibitory receptors. A distinct feature of NK cell activation is that stimulation of resting NK cells with single activating receptor on its own cannot mount natural cytotoxicity. Instead, specific pairs of co-activation receptors are required to unleash NK cell activation via synergy- dependent mechanism. Because each co-activation receptor uses distinct signaling modules, NK cell synergy relies on the integration of such disparate signals. This explains why the study of the mechanism underlying NK cell synergy is important and necessary. Recent studies revealed that NK cell synergy depends on the integration of complementary signals converged at a critical checkpoint element but not on simple amplification of the individual signaling to overcome intrinsic activation threshold. This review focuses on the signaling events during NK cells activation and recent advances in the study of NK cell synergy.

T Cell Immune Responses against SARS-CoV-2 in the With Corona Era

  • Ji-Eun Oh
    • Biomedical Science Letters
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    • v.28 no.4
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    • pp.211-222
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    • 2022
  • After more than two years of efforts to end the corona pandemic, a gradual recovery is starting in countries with high vaccination rates. Easing public health policies for a full-fledged post-corona era, such as lifting the mandatory use of outdoor mask and quarantine measures in entry have been considered in Korea. However, the continuous emergence of new variants of SARS-CoV-2 and limitations in vaccine efficacy still remain challenging. Fortunately, T cells and memory T cells, which are key components of adaptive immunity appear to contribute substantially in COVID-19 control. SARS-CoV-2 specific CD4+/CD8+ T cells are induced by natural infection or vaccination, and rapid induction and activation of T cells is mainly associated with viral clearance and attenuated clinical severity. In addition, T cell responses induced by recognition of a wide range of epitopes were minimally affected and conserved against the highly infectious subsets of omicron variants. Polyfunctional SARS-CoV-2 specific T cell memory including stem cell-like memory T cells were also developed in COVID-19 convalescent patients, suggesting long lasting protective T cell immunity. Thus, a robust T-cell immune response appears to serve as a reliable and long-term component of host protection in the context of reduced efficacy of humoral immunity and persistent mutations and/or immune escape.

The Interaction between HCV-Infected huh7.5 Cells and HCV-Specific T Cells (C형 간염 바이러스 감염 간암 세포주와 T 림프구의 상호작용에 대한 연구)

  • Kang, Hyojeung;Cho, Hyosun
    • Korean Journal of Microbiology
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    • v.50 no.2
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    • pp.169-172
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    • 2014
  • Recently, Hepatitis C virus (HCV) replication system has been established using human hepatoma cells (huh cell) and a variety of HCV clones. In this study, we established an infectious HCV replication system using huh7.5 cells and J6/JFH1 clone (genotype 2a). In addition, we investigated the antigen presentation capability of HCV-infected huh7.5 cells to HCV-specific T cells. Interestingly, HCV-infected huh7.5 cells were not capable of activating HCV-specific T cells. However, huh7.5 cells stimulated by exogenous HCV peptide were able to activate HCV-specific T cells, which was shown to produce TNF-${\alpha}$ and IFN-${\gamma}$. We further examined if HCV infection has an inhibitory effect on the expression of MHC class I molecule of huh7.5 cells. We found that HCV infection did not change the expression level of MHC class I molecule on huh7.5 cells.

A Case of Cytomegalovirus Colitis in Chronic Adult T-Cell Leukemia/Lymphoma (만성 성인T세포백혈병/림프종 환자에서 병발한 거대세포바이러스 장염 1예)

  • Park, Han-Seung;Kim, Dae-Young;Kim, Ji-Beom;Kim, Yun-Ku;Cho, Min-Soo;Ok, Tae-Jin;Jang, Sun-Joo;Lee, Kyoo-Hyung
    • Journal of Yeungnam Medical Science
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    • v.28 no.2
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    • pp.187-191
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    • 2011
  • Adult T-cell leukemia/lymphoma (ATLL) is a malignancy of mature T-cells caused by the human T-cell lymphotrophic virus type I (HTLV-D. HTLV-I is endemic in some areas in Japan, the Caribbean basin, and Africa but has low prevalence in South Korea. Patients with ATLL are susceptible to opportunistic infections such as cytomegalovirus (CMV) infection, but CMV infection in chronic ATLL is uncommon. Reported herein is a case involving a 44-year-old woman with chronic ATLL who presented the symptoms of fever and diarrhea. She was suspected to have acute-type ATLL but was later diagnosed with CMV colitis.

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Changes of Cytokine and Chemokine mRNA Expression in Whole Blood Cells from Active Pulmonary Tuberculosis Patients after T-Cell Mitogen and Mycobacterium tuberculosis Specific Antigen Stimulation

  • Kim, Sunghyun;Park, Sangjung;Lee, Hyeyoung
    • Biomedical Science Letters
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    • v.20 no.3
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    • pp.162-167
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    • 2014
  • Tuberculosis (TB) is one of the major global health problems and it has been estimated that in 5~10% of Mycobacterium tuberculosis (MTB)-infected individuals, the infection progresses to an active disease. Numerous cytokines and chemokines regulate immunological responses at cellular level including stimulation and recruitment of wide range of cells in immunity and inflammation. In the present study, the mRNA expression levels of eight host immune markers containing of IFN-${\gamma}$, TNF-${\alpha}$, IL-2R, IL-4, IL-10, CXCL9, CXCL10, and CXCL11 in whole blood cells from active pulmonary TB patients were measured after T-cell mitogen (PHA) and MTB specific antigens (ESAT-6, CFP-10, and TB7.7). Among the TH1-type factors, IFN-${\gamma}$ mRNA expression was peaked at 4 h, TNF-${\alpha}$ and IL-2R mRNA expression was significantly high at the late time points (24 h) in active TB patients, TH2-type cytokine (IL4 and IL10) mRNA expression levels in both active TB and healthy controls samples did not changed significantly, and the mRNA expression of the three IFN-${\gamma}$-induced chemokines (CXCL9, CXCL10, and CXCL11) were peaked at the late time points (24 h) in active TB patients after MTB specific antigen stimulation. In conclusion, the mRNA expression patterns of the TB-related immune markers in response to the T-cell mitogen (PHA) differed from those in response to MTB specific antigens and these findings may helpful for understanding the relationship between MTB infection and host immune markers in a transcripts level.

Cutaneous Basal Cell Carcinoma Arising in Odontogenic Cutaneous Fistula

  • Kim, Nam Gyun;Kim, Jun Oh;Park, Young Ji;Kim, Jun Sik;Lee, Yoon Jung;Lee, Kyung Suk
    • Archives of Craniofacial Surgery
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    • v.18 no.2
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    • pp.141-144
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    • 2017
  • An odontogenic cutaneous fistula is a pathological communication between the outer skin surface of the face and the oral cavity. Facial cutaneous fistula is a complication of odontogenic infection that is often misdiagnosed with skin infection. We report a rare case, which was diagnosed as basal cell carcinoma based on the biopsy of skin lesions in the patient who had been diagnosed with odontogenic cutaneous fistula. A 64-year-old male patient presented with a cutaneous odontogenic fistula. The patient had undergone surgical extraction of fistula tract and loose tooth before dermatology or plastic surgery consultation. With the biopsy and computed tomography, it was confirmed that fistula and basal cell carcinoma. However, the connection between the fistula and skin cancer was not clear. Positron emission tomography-computed tomography scan was performed and was not detected as other local or distant metastasis. After that, wide excision of the skin lesion was performed. Although skin cancer is not commonly observed, it is necessary to rule out this disease entity by performing biopsy of skin lesions.

Effects of anti-allergic drugs on intestinal mastocytosis and worm expulsion of rats infected with Neodiplostomum seoulense

  • Shin, Eun-Hee;Kim, Tae-Heung;Hong, Sung-Jong;Park, Jae-Hwan;Guk, Sang-Mee;Chai, Jong-Yil
    • Parasites, Hosts and Diseases
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    • v.41 no.2
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    • pp.81-87
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    • 2003
  • The effects of anti-allergic drugs on intestinal mastocytosis and the expulsion of Neodiplostomum seoulense were observed in Sprague-Dawley rats, after oral infection with 500 metacercariae. The drugs used were hydroxyzine (a histamine receptor H$_1$ blocker), cimetidine (a H$_2$ blocker), cyclosporin-A (a helper T-cell suppressant), and prednisolone (a T- and B-cell suppressant). Infected, but untreated controls, and uninfected controls, were prepared. Worm recovery rate and intestinal mastocytosis were measured on weeks 1, 2, 3, 5, and 7 post-infection. Compared with the infected controls, worm expulsion was significantly (P < 0.05) delayed in hydroxyzine- and cimetidine-treated rats, despite mastocytosis being equally marked in the duodenum of all three groups. In the cyclosporin-A- and prednisolone-treated groups, mastocytosis was suppressed, but worm expulsion was only slightly delayed, without statistical significance. Our results suggest that binding of histamine to its receptors on intestinal smooth muscles is more important in terms of the expulsion of N. seoulense from rats than the levels of histamine alone, or mastocytosis.

Role of a Third Extracellular Domain of an Ecotropic Receptor in Moloney Murine Leukemia Virus Infection

  • Bae Eun-Hye;Park Sung-Han;Jung Yong-Tae
    • Journal of Microbiology
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    • v.44 no.4
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    • pp.447-452
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    • 2006
  • The murine ecotropic retroviral receptor has been demonstrated to function as a mouse cationic amino acid transporter 1(mCAT1), and is comprised of multiple membranespanning domains. Feral mouse (Mus dunni) cells are not susceptible to infection by the ecotropic Moloney murine leukemia virus (MoMLV), although they can be infected by other ecotropic murine leukemia viruses, including Friend MLV and Rauscher MLV. The relative inability of MoMLV to replicate in M. dunni cells has been attributed to two amino acids $(V_{214}\;and\;G_{236})$ located within the third extracellular loop of the M. dunni CAT1 receptor (dCAT1). Via the exchange of the third extracellular loop of the mCAT1 cDNA encoding receptor from the permissive mouse and the corresponding portion of cDNA encoding for the nonpermissive M. dunni receptor, we have identified the most critical amino acid residue, which is a glycine located at position 236 within the third extracellular loop of dCAT1. We also attempted to determine the role of the third extracellular loop of the M. dunni CAT1 receptor with regard to the formation of the syncytium. The relationship between dCAT1 and virus-induced syncytia was suggested initially by our previous identification of two MLV isolates (S82F in Moloney and S84A in Friend MLV), both of which are uniquely cytopathic in M. dunni cells. In an attempt to determine the relationship existing between dCAT1 and the virally-induced syncytia, we infected 293-dCAT1 or chimeric dCAT1 cells with the S82F pseudotype virus. The S82F pseudotype virus did not induce the formation of syncytia, but did show increased susceptibility to 293 cells expressing dCATl. The results of our study indicate that S82F-induced syncytium formation may be the result of cell-cell fusion, but not virus-cell fusion.