Academic literature on the topic 'Antigen-specific immune responses'

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Journal articles on the topic "Antigen-specific immune responses"

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Lillard, James W., Prosper N. Boyaka, Dennis D. Taub, and Jerry R. McGhee. "RANTES Potentiates Antigen-Specific Mucosal Immune Responses." Journal of Immunology 166, no. 1 (January 1, 2001): 162–69. http://dx.doi.org/10.4049/jimmunol.166.1.162.

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Gratama, Jan W., Florian Kern, Fabrizio Manca, and Mario Roederer. "Measuring Antigen-Specific Immune Responses, 2008 update." Cytometry Part A 73A, no. 11 (October 22, 2008): 971–74. http://dx.doi.org/10.1002/cyto.a.20655.

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Pira, Giuseppina Li, Florian Kern, Jan Gratama, Mario Roederer, and Fabrizio Manca. "Measurement of antigen specific immune responses: 2006 update." Cytometry Part B: Clinical Cytometry 72B, no. 2 (2007): 77–85. http://dx.doi.org/10.1002/cyto.b.20186.

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Rastogi, Deepa, Chaodong Wang, Xia Mao, Cynthia Lendor, Paul B. Rothman, and Rachel L. Miller. "Antigen-specific immune responses to influenza vaccine in utero." Journal of Clinical Investigation 117, no. 6 (June 1, 2007): 1637–46. http://dx.doi.org/10.1172/jci29466.

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Trollmo, C., S. Gudmundsson, N. Feltelius, S. Rogberg, G. Smedegard, and L. Klareskog. "Sulphasalazine inhibits human antigen-specific immune responses in vivo." Annals of the Rheumatic Diseases 66, no. 4 (September 19, 2006): 481–85. http://dx.doi.org/10.1136/ard.2006.059881.

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Woodham, Andrew W., Ross W. Cheloha, Jingjing Ling, Mohammad Rashidian, Stephen C. Kolifrath, Maia Mesyngier, Joao N. Duarte, et al. "Nanobody–Antigen Conjugates Elicit HPV-Specific Antitumor Immune Responses." Cancer Immunology Research 6, no. 7 (May 23, 2018): 870–80. http://dx.doi.org/10.1158/2326-6066.cir-17-0661.

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Facciabene, Andrea, Luigi Aurisicchio, and Nicola La Monica. "Baculovirus Vectors Elicit Antigen-Specific Immune Responses in Mice." Journal of Virology 78, no. 16 (August 15, 2004): 8663–72. http://dx.doi.org/10.1128/jvi.78.16.8663-8672.2004.

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ABSTRACT To characterize the induction of antigen-specific immune response mediated by baculovirus, vectors expressing the E2 glycoprotein of hepatitis C virus or the carcinoembryonic antigen (CEA) under the control of the cytomegalovirus immediate-early promoter-enhancer were constructed. Additionally, a baculovirus vector encoding the E2 glycoprotein (Bac-G-E2) and expressing vesicular stomatitis virus glycoprotein (VSV-G) in the viral envelope was generated by inserting the VSV-G coding sequence downstream of the polyhedrin promoter. Mice were subjected to intramuscular, intranasal, or subcutaneous inoculations with Bac-E2 and the cellular immune response was monitored by ELISPOT and intracellular staining. Additionally, humoral response was monitored by titrating anti-E2 antibodies. Induction of a measurable anti-E2 T-cell response was observed only after intramuscular injection and was predominantly CD8+ specific. The immunogenic properties of baculovirus as vaccine vector were not restricted to E2 because a CEA-specific CD4+ T-cell response was observed upon intramuscular injection of Bac-CEA. Interestingly, the Bac-G-E2 vector was shown to be a more efficient immunogen than Bac-E2, in view of the 10-fold difference in the minimal dose required to elicit a measurable T-cell response upon intramuscular injection. Induction of inflammatory cytokines such as gamma interferon, tumor necrosis factor alpha, and interleukin-6 was detected as early as 6 h postinjection of Bac-G-E2. Most importantly, both vectors elicited CD8+ T cells with effector function capable of lysing target cells loaded with a hepatitis C virus-specific epitope. Additionally, enhanced NK cytolytic activity was detected in immunized mice. Thus, these results further demonstrate that baculovirus may be considered a useful vector for gene therapy.
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Kapp, Kerstin, Jochen Maul, Arwed Hostmann, Pamela Mundt, Jan C. Preiss, Arlett Wenzel, Andreas Thiel, Martin Zeitz, Reiner Ullrich, and Rainer Duchmann. "Modulation of systemic antigen-specific immune responses by oral antigen in humans." European Journal of Immunology 40, no. 11 (October 19, 2010): 3128–37. http://dx.doi.org/10.1002/eji.201040701.

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Nagafuchi, Shinya, Satoshi Hachimura, Mamoru Totsuka, Takeshi Takahashi, Masao Goto, Takaji Yajima, Tamotsu Kuwata, Sonoko Habu, and Shuichi Kaminogawa. "Dietary Nucleotides Can Up-Regulate Antigen-Specific Th1 Immune Responses and Suppress Antigen-Specific IgE Responses in Mice." International Archives of Allergy and Immunology 122, no. 1 (2000): 33–41. http://dx.doi.org/10.1159/000024356.

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Yang, De, Yuri Postnikov, Yana Li, Poonam Tewary, Gonzalo de la Rosa, Dennis Kliman, Takashi Furusawa, Michael Bustin, Feng Wei, and Joost Oppenheim. "High mobility group nucleosome-binding protein 1 acts as an alarmin critical for the induction of immune response (113.7)." Journal of Immunology 186, no. 1_Supplement (April 1, 2011): 113.7. http://dx.doi.org/10.4049/jimmunol.186.supp.113.7.

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Abstract Alarmins, defined as endogenous mediator(s) capable of promoting the recruitment and activation of antigen-presenting cells (APCs) including dendritic cells (DCs), can potentially promote immunity, however, their essential contribution to the induction immune responses remain to be demonstrated. Here we report the identification of HMGN1 as a novel alarmin that is critical to the induction of antigen-specific immune response. HMGN1 induced DC maturation and recruitment of APCs and activated NF-κB and multiple MAPKs, in a MyD88-dependent manner. HMGN1 promoted antigen-specific immune response upon co-administration with an antigen. Furthermore, knockout of HMGN1 in mice greatly reduced antigen-specific antibody and T cell responses upon intraperitoneal immunization with an antigen using LPS as an adjuvant. The impaired ability of HMGN1 KO mice to mount antigen-specific immune responses was accompanied by both deficient DC recruitment at sites of immunization and reduced production of inflammatory cytokines. Bone marrow chimera experiments revealed that HMGN1 derived from non-leukocytes played a more critical role in the induction of antigen-specific antibody and T cell responses. Thus, HMGN1 acts as a novel alarmin critical for the induction of adaptive immune response.
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Dissertations / Theses on the topic "Antigen-specific immune responses"

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Aubert, Geraldine. "Molecular detection, monitoring and modulation of antigen specific immune responses." Thesis, University College London (University of London), 2004. http://discovery.ucl.ac.uk/1446766/.

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Stem cell transplantati.on (SCT) represents the only curative treatment option for leukaemia. The bone marrow or peripheral blood stem cells transferred in the transplant procedure restore immune functions, allowing the targeting of infected cells or cells expressing tumour antigens. Cytotoxic T lymphocytes (CTL), key mediators of antigen specific killing, were investigated in the context of cytomegalovirus (CMV) infection or chronic myeloid leukaemia (CML). CMV infection after SCT in the absence of effective immunological control or antiviral therapy is a significant cause of morbidity and mortality. HLA-A*0201 tetramer reagents were prepared with three candidate peptides and used to test healthy donor and SCT patient samples. Only T cells binding to the tetramer made with the predominant pp65 epitope (AE42: 495-503) were found for HLA-A*0201 healthy individuals and patients after SCT and correlated with the estimation of the responding T cell population to this peptide as measured by interferon-Tproduction. Parallel tetramer and viral load monitoring of patients at risk of CMV infection after SCT highlighted an inverse correlation between the state of replication of the virus and the number of CMV specific CTL. Presentation of a CML tumour specific peptide epitope in the context of HLA- A*0301 was demonstrated both at the surface of tumour positive cells lines and patient cells. HLA/peptide tetramer reagents were prepared with this peptide and used to screen CML patient samples. Low frequencies of peptide specific CTL were detected in some patients and could be stimulated in vitro. While donor lymphocytes infusions would improve CTL responses after SCT, they also carry the risk of graft versus host disease and may not comprise an effective CTL population targeted to the antigen of interest. A better outcome may be obtained by infusion of enriched and or expanded specific T cell populations. The enrichment, stimulation and expansion of CTL with HLA/peptide tetramer or modified tetramer complexes was examined, using the HLA-A*0201/CMV CTL response as a model. The use of HLA/peptide tetramers to monitor recipients of SCT has implications for the improvement of the treatment of CMV after SCT and the definition of targets and criteria for effective adoptive transfer. Furthermore, the use of HLA/peptide tetramers could be investigated in the assessment of anti-tumour CTL responses, in enhancing existing responses and possibly in inducing primary immune responses to viral pathogens and to tumours.
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Novak, Erik Joseph. "Tracking antigen-specific immune responses in human infection and disease /." Thesis, Connect to this title online; UW restricted, 2001. http://hdl.handle.net/1773/5084.

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Marshall, Fraser Archibald. "Investigation of ES-62 mediated modulation of antigen-specific immune responses." Thesis, University of Glasgow, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.415257.

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Suschak, John J. III. "Characterization of Innate Immune Pathways in DNA Vaccine-Induced, Antigen-Specific Immune Responses: A Dissertation." eScholarship@UMMS, 2014. https://escholarship.umassmed.edu/gsbs_diss/748.

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A major advantage of DNA vaccination is the ability to induce both humoral and cellular immune responses. DNA vaccines are currently used in veterinary medicine, but their tendency to display low immunogenicity in humans has hindered their usage, despite excellent tolerability and safety profiles. Various approaches have been used to improve the immunogenicity of DNA vaccines. Recent human study data re-established the value of DNA vaccines, especially in priming high-level antigen-specific antibody responses. Data suggests that innate immune responses to the DNA vaccine plasmid itself contribute to the immunogenicity of DNA vaccines, however the underlying mechanisms responsible remain unclear. In this dissertation, we investigate the role of innate immunity in shaping antigen-specific adaptive immune responses following DNA vaccination. The current belief is that the cytosolic DNA sensing pathways govern DNA vaccine immunogenicity. To date, only the type I interferon inducing STING/TBK1 regulatory pathway has been identified as required for DNA vaccine immunogenicity. Surprisingly, neither the upstream receptor nor the downstream signaling molecules in this pathway have been characterized. I therefore investigated a candidate cytosolic DNA receptor, as well as the downstream transcription factors required for generation of antigen-specific immune responses. Additionally, the effects of pro-inflammatory signaling on DNA vaccine immunogenicity have yet to be comprehensively studied. Previous studies have only provided indirect evidence for the role of inflammatory v signaling in DNA vaccination. As such, I also investigated the role of the DNA sensing AIM2 inflammasome in DNA vaccination. My data indicates that AIM2 is a key modulator in DNA vaccination via a previously unrecognized connection to type I interferon. Importantly, this marks the first time a DNA vaccine sensor has been identified. Of note, this dissertation represents a departure from many published works in the field. Whereas previous studies have mostly utilized model antigens and only focused on the adaptive immune responses generated, I analyzed the effects on innate immunity as well. Using various innate gene knockout murine models, I quantified antigen-specific humoral and T cell responses, as well as serum cytokine and chemokines following immunization with a clinically relevant DNA vaccine. Overall, this data provides a basis for understanding the mechanisms of DNA vaccination, allowing for the design of more effective vaccines.
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Suschak, John J. III. "Characterization of Innate Immune Pathways in DNA Vaccine-Induced, Antigen-Specific Immune Responses: A Dissertation." eScholarship@UMMS, 2012. http://escholarship.umassmed.edu/gsbs_diss/748.

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A major advantage of DNA vaccination is the ability to induce both humoral and cellular immune responses. DNA vaccines are currently used in veterinary medicine, but their tendency to display low immunogenicity in humans has hindered their usage, despite excellent tolerability and safety profiles. Various approaches have been used to improve the immunogenicity of DNA vaccines. Recent human study data re-established the value of DNA vaccines, especially in priming high-level antigen-specific antibody responses. Data suggests that innate immune responses to the DNA vaccine plasmid itself contribute to the immunogenicity of DNA vaccines, however the underlying mechanisms responsible remain unclear. In this dissertation, we investigate the role of innate immunity in shaping antigen-specific adaptive immune responses following DNA vaccination. The current belief is that the cytosolic DNA sensing pathways govern DNA vaccine immunogenicity. To date, only the type I interferon inducing STING/TBK1 regulatory pathway has been identified as required for DNA vaccine immunogenicity. Surprisingly, neither the upstream receptor nor the downstream signaling molecules in this pathway have been characterized. I therefore investigated a candidate cytosolic DNA receptor, as well as the downstream transcription factors required for generation of antigen-specific immune responses. Additionally, the effects of pro-inflammatory signaling on DNA vaccine immunogenicity have yet to be comprehensively studied. Previous studies have only provided indirect evidence for the role of inflammatory v signaling in DNA vaccination. As such, I also investigated the role of the DNA sensing AIM2 inflammasome in DNA vaccination. My data indicates that AIM2 is a key modulator in DNA vaccination via a previously unrecognized connection to type I interferon. Importantly, this marks the first time a DNA vaccine sensor has been identified. Of note, this dissertation represents a departure from many published works in the field. Whereas previous studies have mostly utilized model antigens and only focused on the adaptive immune responses generated, I analyzed the effects on innate immunity as well. Using various innate gene knockout murine models, I quantified antigen-specific humoral and T cell responses, as well as serum cytokine and chemokines following immunization with a clinically relevant DNA vaccine. Overall, this data provides a basis for understanding the mechanisms of DNA vaccination, allowing for the design of more effective vaccines.
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Masri, S. Hajar. "The role of natural killer T cells in modulating antigen-specific immune responses." Thesis, University of Oxford, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.497047.

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Römer, Christine [Verfasser]. "Role of stroke-induced immunodepression in preventing central nervous system antigen specific immune responses / Christine Römer." Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2015. http://d-nb.info/1068208775/34.

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Salman, Asmaa Mohamed Mohamed. "Investigation of the activation of tumour-specific immune responses by gene therapy strategies using a model tumour antigen." Thesis, University of Birmingham, 2012. http://etheses.bham.ac.uk//id/eprint/3532/.

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Gene directed enzyme prodrug therapy using E.coli the enzyme nitroreductase (NR) to activate the prodrug CB1954, is being developed as an attractive targeted chemotherapy for eradication of localized tumours. In addition to direct killing of NR-expressing tumour cells and potentially also their immediate neighbours via local spread of the activated prodrug, the consequent release of tumour antigens from dying tumour cells has the potential to induce antitumour immune responses. The present study investigates the capacity of NR/CB1954-mediated tumour cell death to activate CD8\(^+\) T cell responses using ovalbumin (OVA), as a model tumour antigen. The transgenic adenocarcinoma mouse prostate tumour cell line (Tramp-C1) was modified to stably express the therapeutic NR gene together OVA. These modified tumour cells were used to seed tumours in mice and OVA-specific T cell responses to gene therapy were investigated. Treatment of mice bearing NR-expressing tumours with CB1954 enhanced expansion of endogenous OVA-specific CD8\(^+\) T cells and marginally enhanced OVA-specific cytotoxic T lymphocyte (CTL) activity, however long-term CD8\(^+\) T cell dependent immunity was insignificant. The possibility of enhancing NR/CB1954-mediated long-term antitumour immune responses by combining with other immunogene therapies namely, 4-1BB costimulatory ligand (4-1BBL) or granulocyte macrophage colony stimulation factor (GM-CSF) was further explored. These combined therapies notably increased the frequency of memory OVA-specific CD8\(^+\) T cell and CTL response in some lymphoid tissue relative to NR/CB1954 monotherapy. One of the obstacles to cancer immunotherapy is the development of T cell anergy early in the course of tumour progression, therefore it was of interest to investigate the potential of NR/CB1954 and 4-1BBL combined tumour therapy to reverse CD8\(^+\) T cells anergy in vivo. This study describes preliminary results showing the effect of this combined therapy on the proliferative and functional responsiveness of anergic CD8\(^+\) T cells. In conclusion, these findings indicate that NR/CB1954-mediated tumour cell death is a weakly immunogenic process that facilitates short-term antitumour CD8\(^+\) T cell responses. Combining NR/CB1954 with intratumoural GM-CSF or 4-1BBL immunotherapy can enhance the frequency and effector function of memory tumour antigen-specific CD8\(^+\) T cells; and thus has the potential to provide long-term antitumour immunity.
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Leligdowicz, Aleksandra Marta. "Evaluation of T lymphocytes in HIV-2 infection in West Africa: The role of antigen-specific immune responses in disease non-progression." Thesis, University of Oxford, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.487285.

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Both HIV-1 and HIV-2 can cause the Acquired Immunodeficiency Syndrome (AIDS), yet the majority of patients infected with HIV-2 are clinically well and most never experience detrimental effects from the infection. Lessons learned from role of the immune system in the long-term non-progression characteristic of HIV-2 infection could offer insight into how a balanced immune response can protect from the immune system destruction associated with HIV-1 infection. The studies presented in this thesis were carried out in a community-based cohort of HIV-2 long-term non-progressors (LTNPs) in rural Guinea Bissau. The initial work (Chapter 3) outlines the first comprehensive analysis of HIV-2-specific immune responses. The data identified Gag as the most immunogenic HIV-2 protein. The magnitude of interferon gamma (IFN-y) generated against Gag was inversely related to virus load (VL). The most frequently recognised HIV-2 peptides clustered within a defined region of Gag with responses to a si~gle peptide associated with low VL. Given this information, the delineation of HIV-2-specific immune responses was focused on this immunodominant region of the HIV-2 proteome. Included in the detailed analysis was the identification of novel HIV-2 epitopes and ex vivo characterisation of HIV-2-specific T cell function (Chapter 4), in vitro characterisation of HIV-2-specific COB T cell clones (Chapter 5), as well as ex vivo phenotypic analysis of HIV-2-specific COB T cells (Chapter 6). Systemic immune activation is a hallmark of disease progression in both HIV-1 and HIV-2 infection. The final chapter (Chapter 7) examines the contribution of HIV-2 plasma antigenaemia to immune system activation which to date was incompletely defined. Cellular and plasma markers of immune activation were related to clinical (VL and CD4 T cell counts), immunological (HIV-2-specific IFN-y secretion) and virus sequence (p26 phenotype) correlates of protection from progression to AIDS. The aim of this work was to understand better what aspects of the host immune response in chronic HIV-2 infection contribute to the relative maintenance of the immune system during the course of this infection.
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O'Brien, Mark Alasdair. "T cell function and MHC-restriction of the equine antigen-specific immune response." Thesis, University of Cambridge, 1992. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.260434.

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Books on the topic "Antigen-specific immune responses"

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The Anatomy of antigen-specific immune responses. Copenhagen: Munksgaard, 1997.

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L, Edelson Richard, ed. Antigen and clone-specific immunoregulation. New York, N.Y: New York Academy of Sciences, 1991.

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Eljaafari, Assia, and Pierre Miossec. Cellular side of acquired immunity (T cells). Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0049.

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The adaptive T-cell response represents the most sophisticated component of the immune response. Foreign invaders are recognized first by cells of the innate immune system. This leads to a rapid and non-specific inflammatory response, followed by induction of the adaptive and specific immune response. Different adaptive responses can be promoted, depending on the predominant effector cells that are involved, which themselves depend on the microbial/antigen stimuli. As examples, Th1 cells contribute to cell-mediated immunity against intracellular pathogens, Th2 cells protect against parasites, and Th17 cells act against extracellular bacteria and fungi that are not cleared by Th1 and Th2 cells. Among the new subsets, Th22 cells protect against disruption of epithelial layers secondary to invading pathogens. Finally these effector subsets are regulated by regulatory T cells. These T helper subsets counteract each other to maintain the homeostasis of the immune system, but this balance can be easily disrupted, leading to chronic inflammation or autoimmune diseases. The challenge is to detect early changes in this balance, prior to its clinical expression. New molecular tools such as microarrays could be used to determine the predominant profile of the immune effector cells involved in a disease process. Such understanding should provide better therapeutic tools to counteract deregulated effector cells.
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van der Vlag, Johan, and Jo H. M. Berden. The patient with systemic lupus erythematosus. Edited by Giuseppe Remuzzi. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0161.

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Systemic lupus erythematosus (SLE) is a systemic autoimmune disease with various clinical manifestations. The hallmark of SLE is the presence of antibodies against nuclear constituents, such as double-stranded (ds)DNA, histones, and nucleosomes. Local deposition of antinuclear antibodies in complex with nuclear autoantigens induces serious inflammatory conditions that can affect several tissues and organs, including the kidney.The levels of antinucleosome and anti-dsDNA antibodies seem to correlate with glomerulonephritis and these autoantibodies can often be detected years before the patient is diagnosed with SLE. Apoptotic debris is present in the extracellular matrix and circulation of patients with SLE due to an aberrant process of apoptosis and/or insufficient clearance of apoptotic cells and apoptotic debris. The non-cleared apoptotic debris in patients with SLE may lead to activation of both the innate (myeloid and plasmacytoid dendritic cells) and adaptive (T and B cells) immune system. In addition to the activation by apoptotic debris and immune complexes, the immune system in SLE may be deregulated at the level of (a) presentation of self-peptides by antigen-presenting cells, (b) selection processes for both B and T cells, and (c) regulatory processes of B- and T-cell responses. Lupus nephritis may be classified in different classes based on histological findings in renal biopsies. The chromatin-containing immune complexes deposit in the capillary filter, most likely due to the interaction of chromatin with the polysaccharide heparan sulphate. A decreased renal expression of the endonuclease DNaseI further contributes to the glomerular persistence of chromatin and the development of glomerulonephritis.Current treatment of lupus nephritis is not specific and aims to reduce the inflammatory response with general immunosuppressive therapies. However, research has revealed novel potential therapeutic candidates at the level of dendritic cells, B cells, and T cells.
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Voll, Reinhard E., and Barbara M. Bröker. Innate vs acquired immunity. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0048.

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The innate and the adaptive immune system efficiently cooperate to protect us from infections. The ancient innate immune system, dating back to the first multicellular organisms, utilizes phagocytic cells, soluble antimicrobial peptides, and the complement system for an immediate line of defence against pathogens. Using a limited number of germline-encoded pattern recognition receptors including the Toll-like, RIG-1-like, and NOD-like receptors, the innate immune system recognizes so-called pathogen-associated molecular patterns (PAMPs). PAMPs are specific for groups of related microorganisms and represent highly conserved, mostly non-protein molecules essential for the pathogens' life cycles. Hence, escape mutants strongly reduce the pathogen's fitness. An important task of the innate immune system is to distinguish between harmless antigens and potentially dangerous pathogens. Ideally, innate immune cells should activate the adaptive immune cells only in the case of invading pathogens. The evolutionarily rather new adaptive immune system, which can be found in jawed fish and higher vertebrates, needs several days to mount an efficient response upon its first encounter with a certain pathogen. As soon as antigen-specific lymphocyte clones have been expanded, they powerfully fight the pathogen. Importantly, memory lymphocytes can often protect us from reinfections. During the development of T and B lymphocytes, many millions of different receptors are generated by somatic recombination and hypermutation of gene segments making up the antigen receptors. This process carries the inherent risk of autoimmunity, causing most inflammatory rheumatic diseases. In contrast, inadequate activation of the innate immune system, especially activation of the inflammasomes, may cause autoinflammatory syndromes.
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Book chapters on the topic "Antigen-specific immune responses"

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Melchers, F. "The Dominance of Antigen-Specific Receptors in Antigen-Specific Immune Responses." In Current Topics in Microbiology and Immunology, 1–3. Berlin, Heidelberg: Springer Berlin Heidelberg, 1993. http://dx.doi.org/10.1007/978-3-642-78253-4_1.

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Reisner, Yair. "Antigen-Specific Immune Responses in Human/Mouse Chimeras." In Human Hematopoiesis in SCID Mice, 105–26. Berlin, Heidelberg: Springer Berlin Heidelberg, 1995. http://dx.doi.org/10.1007/978-3-662-22008-5_6.

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Totsuka, M., S. Furukawa, M. Toda, A. Ametani, and S. Kaminogawa. "Antigen-Specific Inhibition of Immune Responses by Antigen Analogs With a Single Amino Acid Substitution." In Animal Cell Technology: Basic & Applied Aspects, 505–9. Dordrecht: Springer Netherlands, 1997. http://dx.doi.org/10.1007/978-94-011-5746-9_81.

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Hamada, Shigeyuki, Tomohiko Ogawa, Hidetoshi Shimauchi, and Yutaka Kusumoto. "Induction of Mucosal and Serum Immune Responses to a Specific Antigen of Periodontal Bacteria." In Genetically Engineered Vaccines, 71–81. Boston, MA: Springer US, 1992. http://dx.doi.org/10.1007/978-1-4615-3410-5_9.

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Hu, Xintao, Barbara K. Felber, and Antonio Valentin. "Assessing Antigen-Specific Cellular Immune Responses upon HIV/SIV Plasmid DNA Vaccination in the Nonhuman Primate Model." In Methods in Molecular Biology, 113–31. New York, NY: Springer US, 2020. http://dx.doi.org/10.1007/978-1-0716-0872-2_6.

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Beermann, Christopher. "The Adaptive Defense Response: Physiological and Pathological Stimulatory Potential of Food Components in the Antigen-Specific Immune Response." In Food and the Immune System, 99–125. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-031-11523-3_4.

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Askenase, Philip W. "Delayed-Type Hypersensitivity Recruitment of T Cell Subsets via Antigen-Specific Non-IgE Factors or IgE Antibodies: Relevance to Asthma, Autoimmunity and Immune Responses to Tumors and Parasites (Part 1 of 2)." In Regulation and Functional Significance of T-Cell Subsets, 166–88. Basel: KARGER, 1992. http://dx.doi.org/10.1159/000319121.

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Askenase, Philip W. "Delayed-Type Hypersensitivity Recruitment of T Cell Subsets via Antigen-Specific Non-IgE Factors or IgE Antibodies: Relevance to Asthma, Autoimmunity and Immune Responses to Tumors and Parasites (Part 2 of 2)." In Regulation and Functional Significance of T-Cell Subsets, 189–212. Basel: KARGER, 1992. http://dx.doi.org/10.1159/000319122.

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Rempel-Chin, Julia D., Ming Dong Wang, and Kent T. HayGlass. "Effects of rIL-12 Administration on an Antigen Specific Immune Response." In Advances in Experimental Medicine and Biology, 39–41. Boston, MA: Springer US, 1996. http://dx.doi.org/10.1007/978-1-4615-5855-2_6.

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Peine, Kevin J., Naihan Chen, Eric M. Bachelder, and Kristy M. Ainslie. "Drug Delivery Strategies for Tolerogenic Therapy for Autoimmune Diseases in an Antigen-Specific Manner." In Chronic Illness and Long-Term Care, 112–40. IGI Global, 2019. http://dx.doi.org/10.4018/978-1-5225-7122-3.ch007.

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Autoimmune diseases are the result of an improper immune response towards a self-antigen. Predominantly, autoimmune diseases have been treated using therapies that suppress systemic immune responses, which can result in significant side-effects like increased risk of infection and cancer. Alternatively, induction of immune tolerance through antigen-specific therapies can inhibit disease-associated responses without systemic suppression. Previously, immune tolerance has been accomplished by soluble antigen delivery through oral, nasal or sublingual routes. However, these therapies have shown minimal success in clinical settings. In an attempt to increase the efficacy of these therapies, recent work has utilized microparticulate delivery vehicles for the induction of immune tolerance. Microparticles are capable of increasing the solubility and circulation of cargo. In addition, their ability to passively target macrophages and dendritic cells increases their capacity for modulating the immune response. Recent work has shown microparticles fabricated with disease-associated antigens have limited disease progression and severity in animal models of Multiple Sclerosis, Type 1 Diabetes and Rheumatoid Arthritis. Inhibition of disease progression has corresponded with an antigen-specific decrease in inflammatory responses. The emerging field of inducing tolerance through microparticle-based therapies can limit therapeutic side-effects and increase patient quality of life by providing for long-term suppression of autoimmune disorders without compromising systemic immune function.
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Conference papers on the topic "Antigen-specific immune responses"

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Wraith, DC. "SP0151 Switching off unwanted immune responses: the mechanism of antigen-specific immunotherapy with t cell epitopes." In Annual European Congress of Rheumatology, 14–17 June, 2017. BMJ Publishing Group Ltd and European League Against Rheumatism, 2017. http://dx.doi.org/10.1136/annrheumdis-2017-eular.7209.

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Sharabi, Andrew, Christopher Nirschl, Tina Ceccato, Brian Francica, Angela Alme, Thomas Nirschl, Esteban Velarde, Theodore DeWeese, and Charles Drake. "Abstract 635: Antigen-specific immune responses in melanoma using stereotactic radiotherapy combined with anti-PD1 checkpoint blockade." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-635.

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Han, Yanyan, Ye Wu, Chou Yang, Jing Huang, Yabing Guo, Li Liu, Ping Chen, et al. "Abstract 3761: Specific and dynamic tumor antigen-specific immune responses were elicited in patients with hepatocellular carcinoma after cell-based immunotherapy." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-3761.

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Gomez, Bianca P., Connie Wang, Raphael Viscidi, Shiwen Peng, Liangmei He, T. C. WU, and Chein-Fu Hung. "Abstract 478: Strategy to elicit antigen-specific CD8+ T cell -mediated immune responses against a cryptic CTL epitope of merkel cell polyomavirus large T antigen." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-478.

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Lee, Sung Yong, JaeJeong Shim, Kang Kyung Ho, Kye Young Lee, Chien-Fu Hung, and T. C. Wu. "Abstract B33: Endoplasmic reticulum stress enhances the antigen-specific T cell immune responses and therapeutic antitumor effects generated by therapeutic HPV vaccines." In Abstracts: AACR Special Conference: Tumor Immunology and Immunotherapy: A New Chapter; December 1-4, 2014; Orlando, FL. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/2326-6074.tumimm14-b33.

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Chen, Yu-Li, Ming-Cheng Chang, Chia-Yen Huang, Ying-Cheng Chang, Yun-Yuan Chen, Ju-Ming Wang, and Wen-Fang Cheng. "Abstract 3536: Depletion of regulatory T lymphocytes reverses the imbalance between Pro- and anti-tumor immunities via enhancing antigen-specific T cell immune responses." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-3536.

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Krishnakumar, D., and K. S. Jaganathan. "Development of nasal HPV vaccine formulations." In 16th Annual International Conference RGCON. Thieme Medical and Scientific Publishers Private Ltd., 2016. http://dx.doi.org/10.1055/s-0039-1685403.

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Cervical cancer is the second most cancer in women worldwide with over 500000 new cases and 275000 deaths being registered every year. With nearly 73000 women dying every year, India now tops the world in cervical cancer deaths. India represents 26.4% of all women dying of cervical cancer globally. Cervical cancer estimated to be responsible for about 5% of human cancers worldwide. Currently available vaccines may not provide complete protection against all HPV types as the protection is primarily type specific. Furthermore, the available vaccines are delivered via intramuscular route and require three doses and require cold chain supply which increases the cost of vaccine. Therefore a single dose vaccine delivered via non-invasive route (nasal) that protects against multiple HPV types would be a cost effective and better alternative to the currently available HPV vaccines. The main objective of this study was to prepare HPV antigen loaded poly (lactic-co-glycolic acid) (PLGA) and Tri Methyl Chitosan (TMC) coated PLGA microparticles and compare their efficacy as nasal vaccine. The developed formulations were characterized for size, zeta potential, entrapment efficiency, mucin adsorption ability, in vitro and in vivo studies. PLGA microparticles demonstrated negative zeta potential whereas PLGA-TMC microparticles showed higher positive zeta potential. The protein loading efficiency was found as above 80%. Results indicated that PLGA-TMC microparticles demonstrated substantially higher mucin adsorption when compared to PLGA microparticles. HPV antigen encapsulated in PLGA-TMC particles elicited a significantly higher secretory (IgA) immune response compared to that encapsulated in PLGA particles. Present study demonstrates that PLGA-TMC microparticles with specific size range can be a better carrier adjuvant for nasal subunit vaccines. Surface modified PLGA microparticles proved great potential as a nasal delivery system for HPV infections where systemic and mucosal responses are necessary particularly in conditions after viral pathogens invade the host through the mucosal surface.
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Luo, Mengyao, Shamael S. Dastagir, Xuqing Zhang, Andrea Schmidt, Beatriz Marques, Timothy J. Lyford, Billy Blanco, Laurence A. Turka, Thomas J. Wickham, and Tiffany F. Chen. "Abstract PO044: RTX-321, an allogeneic red blood cell-based artificial antigen presenting cell, expressing MHC I-peptide, 4-1BBL and IL-12, engages primary human HPV-specific T cells and boosts other general immune responses." In Abstracts: AACR Virtual Special Conference: Tumor Immunology and Immunotherapy; October 19-20, 2020. American Association for Cancer Research, 2021. http://dx.doi.org/10.1158/2326-6074.tumimm20-po044.

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Abdul-Wahid, Aws, Aaron Prodeus, Marzena Cydzik, Mays Alwash, and Jean Gariepy. "Abstract A029: A vaccine-induced, antigen-specific TH9 immune response blocks tumor cell engraftment." In Abstracts: Second CRI-CIMT-EATI-AACR International Cancer Immunotherapy Conference: Translating Science into Survival; September 25-28, 2016; New York, NY. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/2326-6066.imm2016-a029.

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Schwartz, B. S., and M. C. Monroe. "INCREASED SECRETION OF A FIBRINOLYTIC INHIBITOR BY HUMAN MONONUCLEAR LEUKOCYTES PARALLELS THE PR0COAGULANT RESPONSE TO SPECIFIC ANTIGEN." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644384.

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The presence of fibrin is a characteristic finding of Immune mediated tissue lesions. It is known that peripheral blood mononuclear cells (PBM) express tissue factor in response to recognition of a specific protein antigen. We have found PBM secrete a plasminogen activator (PA) Inhibitor (I) in parallel to expression of tissue factor upon exposure to a sensitizing antigen. Increased PA-I can be detected by Inhibition of urokinase (UK) in an 125I-fibrin plate assay, Inhibition of 125I-plasminogen cleavage, and formation of complexes between 125I-urokinase and UK-I. PA-I secretion is dose dependent, and antigen specific, i.e. a nonsensitizing antigen does not Induce a PA-I response.The PA-I is secreted by monocytes, however the recognition of antigen is a T-cell function. Inhibition of PBM protein or RNA synthesis abrogates the PA-I response. The PA-I appears to be the type 2 Inhibitor, in that 1) it is a much more efficient Inhibitor of UK than of tissue type PA, 2) it is labile in acid and detergent, and 3) it is neutralized by IgG to human placental PA-I, but not by antiserum to PA-I of endothelial cells. It is concluded that PBM respond to a foreign stimulus by elaborating molecules that lead to both the deposition and persistence of ftbrln.
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Reports on the topic "Antigen-specific immune responses"

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Palmer, Guy, Varda Shkap, Wendy Brown, and Thea Molad. Control of bovine anaplasmosis: cytokine enhancement of vaccine efficacy. United States Department of Agriculture, March 2007. http://dx.doi.org/10.32747/2007.7695879.bard.

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Anaplasmosis an arthropod-born disease of cattle caused by the rickettsia Anaplasma marginale and is an impediment to efficient production of healthy livestock in both Israel and the United States. Currently the only effective vaccines are derived from the blood of infected cattle. The risk of widespread transmission of both known and newly emergent pathogens has prevented licensure of live blood-based vaccines in the U.S. and is a major concern for their continued use in Israel. Consequently development of a safe, effective vaccine is a high priority. In this collaborative project we focused on two approaches to vaccine development. The first focused o n improving antigen delivery to livestock and specifically examined how DNA vaccines could be improved to enhance priming and expansion of the immune response. This research resulted in development and testing of two novel vaccine delivery systems--one that targeted antigen spread among dendritic cells (the key cell in priming immune responses and a follow-on construct that also specifically targeted antigen to the endosomal-lysosomal compartment the processing organelle within the dendritic cell that directs vaccine antigen to the MHC class ll-CD4* T cell priming pathway). The optimized construct targeting vaccine antigen to the dendritic cell MHC class II pathway was tested for ability to prime A. marginale specific immune responses in outbred cattle. The results demonstrated both statistically significant effects of priming with a single immunization, continued expansion of the primary immune response including development of high affinity lgG antibodies and rapid recall of the memory response following antigen challenge. This portion of the study represented a significant advance in vaccine delivery for livestock. Importantly the impact of these studies is not limited to A. marginale a s the targeting motifs are optimized for cattle and can be adapted to other cattle vaccinations by inserting a relevant pathogen-specific antigen. The second approach (which represented an addition to the project for which approval was requested as part of the first annual report) was a comparative approach between A . marginale and the Israel A . centrale vaccines train. This addition was requested as studies on Major Surface Protein( MSP)- 2 have shown that this antigen is highly antigenically variable and presented solely as a "static vaccine" antigen does not give cross-strain immunity. In contrast A. . centrale is an effective vaccine which Kimron Veterinary institute has used in the field in Israel for over 50 years. Taking advantage of this expertise, a broad comparison of wild type A. marginale and vaccine strain was initiated. These studies revealed three primary findings: i) use of the vaccine is associated with superinfection, but absence of clinical disease upon superinfection with A. marginale; ii) the A. centrale vaccine strain is not only less virulent but transmission in competent in Dermacentor spp. ticks; and iii) some but not all MSPs are conserved in basic orthologous structure but there are significant polymorphisms among the strains. These studies clearly indicated that there are statistically significant differences in biology (virulence and transmission) and provide a clear path for mapping of biology with the genomes. Based on these findings, we initiated complete genome sequencing of the Israel vaccine strain (although not currently funded by BARD) and plant to proceed with a comparative genomics approach using already sequenced wild-type A. marginale. These findings and ongoing collaborative research tie together filed vaccine experience with new genomic data, providing a new approach to vaccine development against a complex pathogen.
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Baszler, Timothy, Igor Savitsky, Christopher Davies, Lauren Staska, and Varda Shkap. Identification of bovine Neospora caninum cytotoxic T-lymphocyte epitopes for development of peptide-based vaccine. United States Department of Agriculture, March 2006. http://dx.doi.org/10.32747/2006.7695592.bard.

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The goal of the one-year feasibility study was to identify specific cytotoxic T-lymphocyte (CTL) epitopes to Neosporacaninum in the natural bovine host in order to make progress toward developing an effective peptide-based vaccine against bovine neosporosis. We tested the hypothesis that: N. caninum SRS2 peptides contain immunogenicCTLepitope clusters cross-presented by multiple bovine MHC-I and MHC-IIhaplotypes. The specific objectives were: (1) Map bovine CTLepitopes of N. caninum NcSRS-2 and identify consensus MHC-I and class-II binding motifs; and (2) Determine if subunit immunization with peptides containing N. caninum-specificCTLepitopes cross-reactive to multiple bovine MHChaplotypes induces a CTL response in cattle with disparate MHChaplotypes. Neosporosis is a major cause of infectious abortion and congenital disease in cattle, persisting in cattle herds via vertical transmission.5 N. caninum abortions are reported in Israel; a serological survey of 52 Israeli dairy herds with reported abortions indicated a 31% infection rate in cows and 16% infection rate in aborted fetuses.9,14 Broad economic loss due to bovine neosporosis is estimated at $35,000,000 per year in California, USA, and $100,000,000 (Australian) per year in Australia and New Zealand.13 Per herd losses in a Canadian herd of 50 cattle are estimated more conservatively at $2,305 (Canadian) annually.4 Up to date practical measures to reduce losses from neosporosis in cattle have not been achieved. There is no chemotherapy available and, although progress has been made toward understanding immunity to Neospora infections, no efficacious vaccine is available to limit outbreaks or prevent abortions. Vaccine development to prevent N. caninum abortion and congenital infection remains a high research priority. To this end, our research group has over the past decade: 1) Identified the importance of T-lymphocyte-mediated immunity, particularly IFN-γ responses, as necessary for immune protection to congenital neosporosis in mice,1,2,10,11 and 2) Identified MHC class II restricted CD4+ CTL in Neosporainfected Holstein cattle,16 and 3) Identified NcSRS2 as a highly conserved surface protein associated with immunity to Neospora infections in mice and cattle.7,8,15 In this BARD-funded 12 month feasibility study, we continued our study of Neospora immunity in cattle and successfully completed T-lymphocyte epitope mapping of NcSRS2 surface protein with peptides and bovine immune cells,15 fulfilling objective 1. We also documented the importance of immune responses NcSRS2 by showing that immunization with native NcSRS2 reduces congenital Neospora transmission in mice,7 and that antibodies to NcSRS2 specifically inhibition invasion of placental trophoblasts.8 Most importantly we showed that T-lymphocyte responses similar to parasite infection, namely induction of activated IFN-γ secreting Tlymphocytes, could be induced by subunit immunization with NcSRS2 peptides containing the Neospora-specificCTLepitopes (Baszler et al, In preparation) fulfilling objective 2. Both DNA and peptide-based subunit approaches were tested. Only lipopeptide-based NcSRS2 subunits, modified with N-terminal linked palmitic acid to enhance Toll-like receptors 2 and 1 (TLR2-TLR1), stimulated robust antigen-specific T-lymphocyte proliferation, IFN-γ secretion, and serum antibody production across different MHC-IIhaplotypes. The discovery of MHC-II cross-reactive T-cellinducing parasite peptides capable of inducing a potentially protective immune response following subunit immunization in cattle is of significant practical importance to vaccine development to bovine neosporosis. In addition, our findings are more widely applicable in future investigations of protective T-cell, subunit-based immunity against other infectious diseases in outbred cattle populations.
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Knowles, Donald, and Monica Leszkowicz Mazuz. Transfected Babesia bovis expressing the anti-tick Bm86 antigen as a vaccine to limit tick infestation and protect against virulent challenge. United States Department of Agriculture, January 2014. http://dx.doi.org/10.32747/2014.7598160.bard.

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Bovine babesiosis, caused by the apicomplexan parasites Babesiabovisand B. bigemina, is a major tick borne disease of cattle with significant economic importance globally. The vectors of Babesia parasites are R. (Boophilus) annulatusand R. microplus. In Israel these parasites are transmitted manly by R. annulatus. The main goal of the proposal was developing and testing a novel B. bovisvaccine based on stably transfected attenuated B. bovisexpressing the anti-tick Bm86 antigen. This required generating a transfected- attenuated B. bovisparasite containing a bidirectional promoter expressing both, the gfp- bsd selectable marker and the tick vaccine antigen Bm86. The vaccine was tested for its ability to elicit protective immune responses against T. annulatusticks. Efficient control of babesiosis is based on a complex scheme of integrated management, including preventive immunization, anti-babesial chemotherapy and control of tick populations. Live vaccines based on attenuated parasites are the most effective measure to control babesiosis, and are currently used in several countries, including Israel. Live attenuated parasites lead to a chronic infection and development of strong and long term immunity in vaccinated cattle. Still, live vaccines have several limitations, including the difficulty to distinguish among vaccinated and naturally infected cattle and potential for sporadic outbreaks in vaccinated animals. Tick limitation is essential to control babesiosis but the main measure to reduce tick infestation is traditionally approached using acaricides, which is limited by environmental concerns and the development of resistance by the ticks. Alternative tick-control measures including the use of anti-tick vaccines are emerging, and at least partial protective immunity has been achieved against tick vectors by vaccination with recombinant protective tick antigens (ie: Bm86). In addition, the Babesia vaccine development toolbox has been recently expanded with the development of transfection technology in Babesia parasites. In this approved proposal we successfully developed a Babesia live attenuated transfected vaccine, which is able to express a B. bovisMSA-1 signal-Bm86 chimera and eGFP genes under the control of the B. bovisef- 1 and actin promoters respectively. Genetic analysis demonstrated specific stable integration of the transfected genes in the expected ef-1 locus, and immunofluorescence analysis confirmed expression of Bm86 in the surface of transfected parasites. When applied to splenectomized calves, the transfected parasites were able to cause persistent B. bovisinfection with production of antibodies reactive with Bm86 for at least six months. In addition, partial protection against ticks was also observed upon challenging the vaccinated animals with R. annulatuslarvae. However, when used on intact calves, the vaccine failed to elicit detectable immune responses against Bm86, and we are still in the process of interpreting the data and make necessary changes in our experimental approaches. Overall, the results obtained here represent a step forward towards the development of integrated vaccines against both ticks and tick –borne pathogens, using the Babesia attenuated parasites as a platform to the delivery of exogenous protective antigens
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McElwain, Terry, Eugene Pipano, Guy Palmer, Varda Shkap, Stephen Hines, and Douglas Jasmer. Protection of Cattle Against Babesiosis: Immunization with Recombinant DNA Derived Apical Complex Antigens of Babesia bovis. United States Department of Agriculture, June 1995. http://dx.doi.org/10.32747/1995.7612835.bard.

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Bovine babesiosis caused by Babesia bovis continues to be a significant deterrent to global livestock production. Current control methods have both biological and technical drawbacks that have stimulated research on improved methods of vaccination. This BARD project has focused on characterization of candidate Babesia bovis vaccine antigens located in the apical complex, a unique group of subcellular organelles - including rhoptries, micronemes, and spherical bodies - involved in the invation of erythrocytes. Spherical bodies and rhoptries were partially purified and their contents characterized using monoclonal antibodies. Existing and newly developed monoclonal antibodies bound to antigens in the spherical body, rhoptry, merozoite membrane, and infected erythrocyte membrane. In an initial immunization study using biologically cloned strains, it was demonstrated that strain-common epitopes are important for inducing immune protection against heterologous challenge. Rhoptry-associated antigen 1 (RAP-1) had been demonstrated previously to induce partial immune protection, fulfilled criteria of broad interstrain B and T cell epitope conservation, and thus was further characterized. The RAP-1 gene family consists of at least two gene copies, is homologous to the RAP-1 gene family in B. bigemina, and contains significant sequence similarity to other erythroparasitic protozoan candidate vaccine antigens, including the apical membrane antigen of Plasmodium falciparum. A new RAP-1 monoclonal antibody was developed that inhibits merozoite growth in vitro, demonstrating the presence of a RAP-1 neutralization sensitive domain. Based on these observations, cattle were immunized with Mo7 (Mexico) strain recombinant RAP-1 representing one of the two gene copies. All cattle responded with variable levels of serum antibodies inhibitory to heterologous Israel strain merozoite growth in vitro, and RAP-1 specific T lymphocytes that proliferated when stimulated with either homologous or heterologous native parasite antigen. Minimal protection from clinical disease was present after virulent Israel (heterologous) strain B. bovis challenge. In total, the results support the continued development of RAP-1 as a vaccine antigen, but indicate that additional information about the native structure and function of both RAP-1 gene copies, including the relationship of conserved and polymorphic sequences to B and T cell lepitopes relevant for protection, is necessary for optimization of RAP-1 as a vaccine component.
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