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Search Results: 1 - 10 of 2497 matches for " immune-evasion "
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Immune Evasion Strategies of Ranaviruses and Innate Immune Responses to These Emerging Pathogens
Leon Grayfer,Francisco De Jesús Andino,Guangchun Chen,Gregory V. Chinchar,Jacques Robert
Viruses , 2012, DOI: 10.3390/v4071075
Abstract: Ranaviruses (RV, Iridoviridae) are large double-stranded DNA viruses that infect fish, amphibians and reptiles. For ecological and commercial reasons, considerable attention has been drawn to the increasing prevalence of ranaviral infections of wild populations and in aquacultural settings. Importantly, RVs appear to be capable of crossing species barriers of numerous poikilotherms, suggesting that these pathogens possess a broad host range and potent immune evasion mechanisms. Indeed, while some of the 95–100 predicted ranavirus genes encode putative evasion proteins (e.g., vIFα, vCARD), roughly two-thirds of them do not share significant sequence identity with known viral or eukaryotic genes. Accordingly, the investigation of ranaviral virulence and immune evasion strategies is promising for elucidating potential antiviral targets. In this regard, recombination-based technologies are being employed to knock out gene candidates in the best-characterized RV member, Frog Virus (FV3). Concurrently, by using animal infection models with extensively characterized immune systems, such as the African clawed frog, Xenopus laevis, it is becoming evident that components of innate immunity are at the forefront of virus-host interactions. For example, cells of the macrophage lineage represent important combatants of RV infections while themselves serving as targets for viral infection, maintenance and possibly dissemination. This review focuses on the recent advances in the understanding of the RV immune evasion strategies with emphasis on the roles of the innate immune system in ranaviral infections.
Periodontal Disease: General Aspects from Biofilm to the Immune Response Driven by Periodontal Pathogens  [PDF]
Giovanna R. Degasperi, Augusto Etchegaray, Larissa Marcelino, Ahron Sicard, Karina Villalpando, Sérgio L. Pinheiro
Advances in Microbiology (AiM) , 2018, DOI: 10.4236/aim.2018.81001
Abstract: Periodontal disease is of inflammatory origin and affects the dental support tissues. The initial phase is characterized by the accumulation of biofilm, which is a predisposing factor for several oral pathologies. The combination of extrinsic factors such as lack of hygiene, smoking and diet, and intrinsic factors such as genetics, and major changes in the immune response associated with immune escape mechanisms of biofilm constituents are crucial to the development and progression of the disease, which when untreated entails local irreversible consequences that can lead to systemic changes. In this brief review, we describe general aspects of periodontal disease, its risk factors and ways of preventing the disease. In particular, we discuss some of the mechanisms of immune response to periodontal pathogens, as well as the escape mechanisms of these microorganisms.
Role of apoptosis resistance in immune evasion and metastasis of colorectal cancer
Kebin Liu
World Journal of Gastrointestinal Oncology , 2010,
Abstract: The host immune system functions as a guardian against tumor development. It has been demonstrated that cytotoxic T lymphocyte (CTL)-mediated cytotoxic pathways function to inhibit or delay human colorectal cancer development. However, the host anti-tumor immune responses also 'edit' the tumor and select for more aggressive variants, resulting in immune evasion and tumor escape. Fas is a death receptor that mediates one of the major cytotoxic effector mechanisms of the CTLs. Fas is highly expressed in normal human colon epithelial cells but is frequently silenced in colorectal carcinoma, especially in metastatic colorectal carcinoma, suggesting that loss of Fas expression and function may be an immune evasion and tumor escape mechanism. In addition, recent studies indicated that Fas also mediates cellular proliferation signaling pathways to promote tumor development. Therefore, the death receptor Fas may not only transduce death signals to suppress tumor development but also activate cellular proliferation and the migration process to promote tumor growth and progression. Thus, understanding the mechanisms by which the Fas receptor and its associated protein complex transduces the death and survival signals may identify molecular targets for the development of therapeutic strategy to enhance the Fas-mediated death signals to increase the efficacy of cancer immunotherapy.
Immune Evasion of Human Lung Carcinoma Cell A549 Suppressed by Human Lymphoma Cell Jurkat via Fas/FasL Pathway
Hongmei WANG,Guoqiang ZHANG,Jigang DAI,Jiaxin MIN
Chinese Journal of Lung Cancer , 2010,
Abstract: Background and objective Tumor escape from the host immune system has been a major problem in immunotherapy of human malignancies. FasL/Fas-induced apoptosis plays an important role in various immunological processes. The aim of this study is to investigate the immune evasion in human lung carcinoma cell A549 induced by human lymphoma cell Jurkat via Fas/FasL pathway. Methods Jurkat cells and A549 cells were co-cultured at different proportions. The apoptotic rates of A549 cells were determined by flow cytometry (FCM). Protein levels of Fas, FasL and Caspase-8 in A549 cells were detected by Western blot. Results Survival rates of A549 cells gradually decreased and apoptotic rates of A549 cells were significantly enhanced along with ratio increasing between Jurkat and A549. Meanwhile, the protein levels of Fas and Caspase-8 gradually increased in A549 cells, and the protein levels of FasL had no significant difference in all groups. Conclusion The Jurkat cells might decrease the survival rates of A549 cells and enhanced its apoptosis and immune evasion partly via Fas/FasL pathway.
The Status of Research on Mechanisills of Schistosome Immune Evasion

向会耀, 王劲松, 方华舟
Advances in Microbiology (AMB) , 2013, DOI: 10.12677/AMB.2013.21006
The immune evasion of schistosome is an important factor for schistosome survival in host. At present, the mechanism of the immune evasion is known as antigenic change and immune regulation. Antigen changes mainly include Schistosoma antigen variation, simulation and disguise which reduces the sensiticity of immunologic surveillance function of the host. The sehistosome blocks complement activation of the host and suppresses immune cell function of the host by synthetizing neural molecules, protease, cytokines and other small molecules, resulting in immune function down-regulated of the host.
Hepatitis C Virus Evasion Mechanisms from Neutralizing Antibodies
Caterina Di Lorenzo,Allan G. N. Angus,Arvind H. Patel
Viruses , 2011, DOI: 10.3390/v3112280
Abstract: Hepatitis C virus (HCV) represents a major public health problem, affecting 3% of the world’s population. The majority of infected individuals develop chronic hepatitis, which can progress to cirrhosis and hepatocellular carcinoma. To date, a vaccine is not available and current therapy is limited by resistance, adverse effects and high costs. Although it is very well established that cell-mediated immunity is necessary for viral clearance, the importance of host antibodies in clearing HCV infection is being increasingly recognized. Indeed, recent studies indicate that neutralizing antibodies are induced in the early phase of infection by patients who subsequently clear viral infection. Conversely, patients who do not clear the virus develop high titers of neutralizing antibodies during the chronic stage. Surprisingly, these antibodies are not able to control HCV infection. HCV has therefore developed mechanisms to evade immune elimination, allowing it to persist in the majority of infected individuals. A detailed understanding of the mechanisms by which the virus escapes immune surveillance is therefore necessary if novel preventive and therapeutic treatments have to be designed. This review summarizes the current knowledge of the mechanisms used by HCV to evade host neutralizing antibodies.
Activation of the Antiviral Kinase PKR and Viral Countermeasures
Bianca Dauber,Thorsten Wolff
Viruses , 2009, DOI: 10.3390/v1030523
Abstract: The interferon-induced double-stranded (ds)RNA-dependent protein kinase (PKR) limits viral replication by an eIF2α-mediated block of translation. Although many negative-strand RNA viruses activate PKR, the responsible RNAs have long remained elusive, as dsRNA, the canonical activator of PKR, has not been detected in cells infected with such viruses. In this review we focus on the activating RNA molecules of different virus families, in particular the negative-strand RNA viruses. We discuss the recently identified non-canonical activators 5’-triphosphate RNA and the vRNP of influenza virus and give an update on strategies of selected RNA and DNA viruses to prevent activation of PKR.
Filoviral Immune Evasion Mechanisms
Parameshwaran Ramanan,Reed S. Shabman,Craig S. Brown,Gaya K. Amarasinghe,Christopher F. Basler,Daisy W. Leung
Viruses , 2011, DOI: 10.3390/v3091634
Abstract: The Filoviridae family of viruses, which includes the genera Ebolavirus (EBOV) and Marburgvirus (MARV), causes severe and often times lethal hemorrhagic fever in humans. Filoviral infections are associated with ineffective innate antiviral responses as a result of virally encoded immune antagonists, which render the host incapable of mounting effective innate or adaptive immune responses. The Type I interferon (IFN) response is critical for establishing an antiviral state in the host cell and subsequent activation of the adaptive immune responses. Several filoviral encoded components target Type I IFN responses, and this innate immune suppression is important for viral replication and pathogenesis. For example, EBOV VP35 inhibits the phosphorylation of IRF-3/7 by the TBK-1/IKKε kinases in addition to sequestering viral RNA from detection by RIG-I like receptors. MARV VP40 inhibits STAT1/2 phosphorylation by inhibiting the JAK family kinases. EBOV VP24 inhibits nuclear translocation of activated STAT1 by karyopherin-α. The examples also represent distinct mechanisms utilized by filoviral proteins in order to counter immune responses, which results in limited IFN-α/β production and downstream signaling.
Manipulation of NKG2D ligands by cytomegaloviruses: impact on innate and adaptive immune response
Stipan Jonji?
Frontiers in Immunology , 2011, DOI: 10.3389/fimmu.2011.00085
Abstract: NKG2D is a potent activating receptor expressed on NK cells, NKT cells, γδ T cells, and CD8 T cells. NKG2D recognizes cell surface molecules structurally related to MHC class I proteins induced by infection or other type of cellular stress. The engagement of NKG2D leads to NK cell cytotoxicity and cytokine secretion or to a co-stimulation of CD8 T cells. Both human and mouse cytomegalovirus (CMV) have evolved numerous mechanisms to evade NKG2D-mediated immune response. This review describes the mechanisms used by CMV to inhibit NKG2D ligand expression and the recent advances in exploiting the NKG2D recognition pathway for mounting efficient and long-lasting immune response.
Immune evasion by Plasmodium falciparum parasites: converting a host protection mechanism for the parasite′s benefit  [PDF]
Bismarck Dinko, Gabriele Pradel
Advances in Infectious Diseases (AID) , 2016, DOI: 10.4236/aid.2016.62011
Abstract: Immune evasion is a strategy used by pathogenic microbes to evade the host immune system in order to ensure successful propagation. Immune evasion is particularly important for the blood stages of Plasmodium falciparum, the causative agent of the deadly disease malaria tropica. Because Plasmodium blood stage parasites require human erythrocytes for replication, their ability to evade attack by the human immune system is essential for parasite survival. In order to escape immunity-induced killing, the intraerythrocytic parasites have evolved a variety of evasion mechanisms, including expansion of plasmodial surface proteins, organ-specific sequestration of the infected red blood cells and acquisition of immune-regulatory proteins by the parasite. This review aims to highlight recent advances in the molecular understanding of the immune evasion strategies by P. falciparum, including antigenic variation, surface protein polymorphisms and invasion ligand diversification. The review will further discuss new findings on the regulatory mechanisms applied by P. falciparum to avoid lysis by the human complement as well as killing by immune factors of the mosquito vector.
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