Academic literature on the topic 'Protective antibodies'

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Journal articles on the topic "Protective antibodies"

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Vinson, Valda. "Protective neutralizing antibodies." Science 369, no. 6506 (August 20, 2020): 930.13–932. http://dx.doi.org/10.1126/science.369.6506.930-m.

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Cherry, James D., Erik L. Hewlett, and Edward A. Mortimer. "Protective antibodies in pertussis." Journal of Pediatrics 117, no. 2 (August 1990): 347. http://dx.doi.org/10.1016/s0022-3476(05)80580-3.

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Li, Hao, Xing-xing Wang, Bin Wang, Lei Fu, Guan Liu, Yu Lu, Min Cao, Hairong Huang, and Babak Javid. "Latently and uninfected healthcare workers exposed to TB make protective antibodies against Mycobacterium tuberculosis." Proceedings of the National Academy of Sciences 114, no. 19 (April 24, 2017): 5023–28. http://dx.doi.org/10.1073/pnas.1611776114.

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The role of Igs in natural protection against infection by Mycobacterium tuberculosis (Mtb), the causative agent of TB, is controversial. Although passive immunization with mAbs generated against mycobacterial antigens has shown protective efficacy in murine models of infection, studies in B cell-depleted animals only showed modest phenotypes. We do not know if humans make protective antibody responses. Here, we investigated whether healthcare workers in a Beijing TB hospital—who, although exposed to suprainfectious doses of pathogenic Mtb, remain healthy—make antibody responses that are effective in protecting against infection by Mtb. We tested antibodies isolated from 48 healthcare workers and compared these with 12 patients with active TB. We found that antibodies from 7 of 48 healthcare workers but none from active TB patients showed moderate protection against Mtb in an aerosol mouse challenge model. Intriguingly, three of seven healthcare workers who made protective antibody responses had no evidence of prior TB infection by IFN-γ release assay. There was also good correlation between protection observed in vivo and neutralization of Mtb in an in vitro human whole-blood assay. Antibodies mediating protection were directed against the surface of Mtb and depended on both immune complexes and CD4+ T cells for efficacy. Our results indicate that certain individuals make protective antibodies against Mtb and challenge paradigms about the nature of an effective immune response to TB.
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Flemming, Alexandra. "Viral vector delivers protective antibodies." Nature Reviews Drug Discovery 12, no. 8 (July 19, 2013): 580. http://dx.doi.org/10.1038/nrd4079.

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Gozdas, Hasan Tahsin, and Oguz Karabay. "Protective effect of tetanus antibodies." American Journal of Emergency Medicine 32, no. 9 (September 2014): 1128. http://dx.doi.org/10.1016/j.ajem.2014.05.009.

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Nussbaum, G., R. Yuan, A. Casadevall, and M. D. Scharff. "Immunoglobulin G3 blocking antibodies to the fungal pathogen Cryptococcus neoformans." Journal of Experimental Medicine 183, no. 4 (April 1, 1996): 1905–9. http://dx.doi.org/10.1084/jem.183.4.1905.

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Vaccination and infection can elicit protective and nonprotective antibodies to the fungus Cryptococcus neoformans in mice. The effect of nonprotective antibodies on host defense is unknown. In this study we used mixtures of protective and nonprotective monoclonal antibodies (mAbs) to determine if nonprotective mAbs blocked the activity of the protective mAbs. Antibody isotype and epitope specificity are important in determining the ability to prolong survival in mice given a lethal C. neoformans infection. Three different nonprotective immunoglobulin (Ig) G23 mAbs to cryptococcal capsular polysaccharide were used to study the interaction between the IgG3 isotype and protective IgG1 and IgG2a mAbs in murine cryptococcal infection. One IgG3 mAb reduced the protective efficacy of an IgG1 with identical epitope specificity. A second IgG3 mAb with different epitope specificity also reduced the protection provided by the IgG1 mAb. The protective efficacy of an IgG2a mAb was also dramatically decreased by still another IgG3 mAb. To our knowledge this is the first report of blocking antibodies to a fungal pathogen. The results have important implications for the development of vaccines and passive antibody therapy against C. neoformans.
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Danelli, Maria das Graças M., Lúcia M. Teixeira, Luiz Carlos D. Formiga, and J. Mauro Peralta. "Protective monoclonal antibodies to diphtheria toxin." Memórias do Instituto Oswaldo Cruz 86, no. 2 (June 1991): 265–67. http://dx.doi.org/10.1590/s0074-02761991000200017.

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Nosanchuk, J. "Protective Antibodies and Endemic Dimorphic Fungi." Current Molecular Medicine 5, no. 4 (June 1, 2005): 435–42. http://dx.doi.org/10.2174/1566524054022530.

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Hjelt, K., and P. C. Grauballe. "Protective Levels of Intestinal Rotavirus Antibodies." Journal of Infectious Diseases 161, no. 2 (February 1, 1990): 352–53. http://dx.doi.org/10.1093/infdis/161.2.352.

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Maamary, Jad, Taia T. Wang, Gene S. Tan, Peter Palese, and Jeffrey V. Ravetch. "Increasing the breadth and potency of response to the seasonal influenza virus vaccine by immune complex immunization." Proceedings of the National Academy of Sciences 114, no. 38 (September 5, 2017): 10172–77. http://dx.doi.org/10.1073/pnas.1707950114.

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The main barrier to reduction of morbidity caused by influenza is the absence of a vaccine that elicits broad protection against different virus strains. Studies in preclinical models of influenza virus infections have shown that antibodies alone are sufficient to provide broad protection against divergent virus strains in vivo. Here, we address the challenge of identifying an immunogen that can elicit potent, broadly protective, antiinfluenza antibodies by demonstrating that immune complexes composed of sialylated antihemagglutinin antibodies and seasonal inactivated flu vaccine (TIV) can elicit broadly protective antihemagglutinin antibodies. Further, we found that an Fc-modified, bispecific monoclonal antibody against conserved epitopes of the hemagglutinin can be combined with TIV to elicit broad protection, thus setting the stage for a universal influenza virus vaccine.
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Dissertations / Theses on the topic "Protective antibodies"

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Dillon, David. "Protective antibodies in normal pregnancy." Thesis, University of Aberdeen, 1989. http://digitool.abdn.ac.uk/R?func=search-advanced-go&find_code1=WSN&request1=AAIU028047.

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The aim of this study was to examine the maternal immune response to paternal antigens expressed by the fetus and identify the antigen inducing the response. Sera removed from responder female mice were tested for activity against paternal target cells using a cellular ELISA. Avtivity was first detectable at day 10 of a first pregnancy. The antibody detected in this way was shown to be non-cytotoxic, consisting of the IgGl subclass, directed against a class I antigen that could not be found on target erythrocytes. Sera removed at different stages of pregnancy exhibited varying degrees of cross-reactivity. To provide a source of pregnancy-induced antibody spleens from mice were removed during pregnancy and fused with rat or mouse myelomas. Antibody-secreting hybridomas were sought by means of CELISA with paternal cells as targets. Four hybridomas were isolated, producing antibody of the IgGl subclass, directed against a class I antigen and with limited cross-reactivity. The target antigen for both pregnancy sea and monoclonal antibody was examined for H-2 linkage, using the Lod score. The results obtained were unusual. Combination of the scores for four separate sera suggested an MHC-linked target. Individual scores suggested that two sera were directed against a linked and two against an unlinked antigen. Three of the monoclonal antidbodies were directed against H-2-linked antigens. Both sera and monoclonal antibody were immunoblotted against paternal, maternal and control cells. Pregnancy sera was seen to blot a 45-kD antigen present on paternal strain cells and cells from a mouse sharing the maternal haplotype. Only one hybridoma could be successfully blotted, revealing a 45-kD target. Immunisation with third-party lymphocytes has been used to treat recurrent spontaneous abortion. In twenty two couples treated in this way immunisation proved to be beneficial but there was no evidence for importance of an immune response or HLA sharing.
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Parker, Christopher S. "Effect of a codon optimized DNA prime on induction of anti-influenza protective antibodies." Worcester, Mass. : Worcester Polytechnic Institute, 2007. http://www.wpi.edu/Pubs/ETD/Available/etd-040907-100839/.

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Berry, P. R. "Production of monoclonal antibodies to Bordetella pertussis as a means of identifying protective antigens." Thesis, University of Reading, 1987. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.376819.

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Figueroa, Z. E. F. "Specificity and protective effect of polyclonal antibodies to antigens of Plasmodium berghei and Plamodium chabaudi." Thesis, Open University, 1985. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.304217.

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Czifra, György. "Identification of Mycoplasma gallisepticum antigens with diagnostic and protective properties /." Uppsala : Swedish Univ. of Agricultural Sciences (Sveriges lantbruksuniv.), 1999. http://epsilon.slu.se/avh/1999/91-576-5900-1.pdf.

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Mugyenyi, Cleopatra Kama. "The acquisition and maintenance of antibodies to merozoite antigens of Plasmodium falciparum and their role in protective immunity to malaria." Thesis, Open University, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.522224.

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Murugan, Rajagopal. "Protective memory B cell response in controlled human malaria infection." Doctoral thesis, Humboldt-Universität zu Berlin, 2019. http://dx.doi.org/10.18452/19695.

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Antikörper gegen Circumsporozoite protein (CSP), ein Oberflächenantigen von Plasmodium falciparum (Pf), können sterile Immunität hervorrufen und dadurch die Entwicklung von Malaria im Tierversuch verhindern. Im Menschen werden protektive B-Zell Gedächtnisantworten gegen CSP durch natürliche Malariaerkrankung bzw. Vakzinierung jedoch nur unzureichend erzeugt. - Für die Entwicklung von Gedächtnis-B-Zellen stellt die Affinitätsreifung, welche durch somatische Immungobulin Hypermutation sowie der nachfolgenden Selektion von B-Zellen mit verbesserter Antigenaffinität charakterisiert ist, eine Schlüsselfunktion in der Generierung von protektiven Immunantworten dar. Wie Affinitätsreifung gegen CSP im Menschen stattfindet ist jedoch nicht bekannt. In dieser Arbeit wird die Affinitätsreifung von CSP Gedächtnis B-Zellen auf Einzelzellebene im Menschen über drei kontrollierte Infektionen mit Pf Sporozoiten unter Chemoprophylaxe untersucht. Durch Hochdurchsatz-Einzelzell-Sequenzierung der Immunoglobulin (Ig) gene loci und der Produktion von rekombinanten monoklonalen Antikörpern gewährt diese Arbeit Einsicht in die Selektion und Affinitätsreifung von humanen Gedächtnis-B-Zell Antworten gegen komplexe Proteinantigene und identifiziert Keimbahn kodierte Immunglobulin Charakteristika, die mit hoher CSP-Affinität und Pf-Inhibition einhergehen. Überraschenderweise zeigen die Daten, dass initiale klonale Selektion von hochaffinen B Zellen eine weitaus wichtigere Rolle als Affinitätsreifung in dieser Infektion spielt. Diese Arbeit zeigt fundamentale Eigenschaften von humanen Gedächtnisantworten in einer komplexen Parasiteninfektion und liefert die Grundlage für ein mögliches Design von neuartigen Immunogenen um hoch-affine B-Zellen gegen CSP effizienter zu induzieren.
Antibodies against the major Plasmodium falciparum (Pf) sporozoite surface protein, circumsporozoite protein (CSP), can mediate sterile immunity thereby preventing malaria disease symptoms as shown by passive transfer in animal models. However, protective anti- CSP memory antibody responses are not efficiently induced by natural Pf exposure or vaccination. Affinity maturation, i.e. the diversification of antigen-activated naïve precursor B cells by a somatic immunoglobulin (Ig) gene mutation process and the subsequent selection of B cells expressing antigen receptors with improved antigen affinity in germinal center reactions is considered key to the formation of protective memory B cell responses. However, how the anti-PfCSP memory B cell response matures in humans is not known. To address this question, the clonal evolution of the human anti-Pf CSP memory B cell response over three successive controlled Pf infections under chemoprophylaxis was assessed at single cell level by high throughput paired full-length Ig gene sequencing and recombinant monoclonal antibody production. The work provides basic insights in the longitudinal development of human memory B cell responses and identified germline-encoded Ig gene features that were associated with high anti-CSP affinity and Pf inhibitory antibody activity. The clonal selection of germline B cells expressing such antibodies, rather than affinity maturation, was associated with high quality anti-PfCSP memory B cell responses. The data provide insights into the evolution of antibody response to a complex protein antigen during infection and a strong rational for the design of novel CSP immunogens to target naïve B cell precursors expressing potent anti-CSP antibodies for the induction of protective memory B cell responses by vaccination.
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Anthony, Robert McCullough. "Characterization and function of the inflammatory response to infection by a gastrointestinal nematode parasite : new insights into protective Th2 responses /." Download the dissertation in PDF, 2006. http://www.lrc.usuhs.mil/dissertations/pdf/Anthony2006.pdf.

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Dumke, Roger, and Enno Jacobs. "Antibody response to Mycoplasma pneumoniae: protection of host and influence on outbreaks?" Saechsische Landesbibliothek- Staats- und Universitaetsbibliothek Dresden, 2017. http://nbn-resolving.de/urn:nbn:de:bsz:14-qucosa-213646.

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In humans of all ages, the cell wall-less and genome-reduced species Mycoplasma pneumoniae can cause infections of the upper and lower respiratory tract. The well-documented occurrence of major peaks in the incidence of community-acquired pneumonia cases reported world-wide, the multifaceted clinical manifestations of infection and the increasing number of resistant strains provide reasons for ongoing interest in the pathogenesis of mycoplasmal disease. The results of recent studies have provided insights into the interaction of the limited virulence factors of the bacterium with its host. In addition, the availability of complete M. pneumoniae genomes from patient isolates and the development of proteomic methods for investigation of mycoplasmas have not only allowed characterization of sequence divergences between strains but have also shown the importance of proteins and protein parts for induction of the immune reaction after infection. This review focuses on selected aspects of the humoral host immune response as a factor that might influence the clinical course of infections, subsequent protection in cases of re-infections and changes of epidemiological pattern of infections. The characterization of antibodies directed to defined antigens and approaches to promote their induction in the respiratory mucosa are also preconditions for the development of a vaccine to protect risk populations from severe disease due to M. pneumoniae.
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Dumke, Roger, and Enno Jacobs. "Antibody response to Mycoplasma pneumoniae: protection of host and influence on outbreaks?" Frontiers Media, 2016. https://tud.qucosa.de/id/qucosa%3A29946.

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In humans of all ages, the cell wall-less and genome-reduced species Mycoplasma pneumoniae can cause infections of the upper and lower respiratory tract. The well-documented occurrence of major peaks in the incidence of community-acquired pneumonia cases reported world-wide, the multifaceted clinical manifestations of infection and the increasing number of resistant strains provide reasons for ongoing interest in the pathogenesis of mycoplasmal disease. The results of recent studies have provided insights into the interaction of the limited virulence factors of the bacterium with its host. In addition, the availability of complete M. pneumoniae genomes from patient isolates and the development of proteomic methods for investigation of mycoplasmas have not only allowed characterization of sequence divergences between strains but have also shown the importance of proteins and protein parts for induction of the immune reaction after infection. This review focuses on selected aspects of the humoral host immune response as a factor that might influence the clinical course of infections, subsequent protection in cases of re-infections and changes of epidemiological pattern of infections. The characterization of antibodies directed to defined antigens and approaches to promote their induction in the respiratory mucosa are also preconditions for the development of a vaccine to protect risk populations from severe disease due to M. pneumoniae.
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Books on the topic "Protective antibodies"

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Felix, Milgrom, Abeyounis C. J, and Albini Boris, eds. Antibodies: Protective, destructive, and regulatory role : 9th International Convocation on Immunology, Amherst, N.Y., June 25-28, 1984. Basel: Karger, 1985.

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Zimmer, Franz-Josef. Protecting and enforcing life science inventions in Europe under EPC and EU law: From antibodies to zebrafish. 2nd ed. München, Germany: C.H. Beck, 2015.

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Milgrom, F. Antibodies: Protective, Destructive and Regulatory Role. S Karger Pub, 1985.

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Ward, Lucy Ann. Protection and immune regulation by circulating, maternally-derived antibodies in neonatal swine infected with rotavirus. 1994.

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Vaheri, Antti, James N. Mills, Christina F. Spiropoulou, and Brian Hjelle. Hantaviruses. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780198570028.003.0035.

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Hantaviruses (genus Hantavirus, family Bunyaviridae) are rodent- and insectivore-borne zoonotic viruses. Several hantaviruses are human pathogens, some with 10-35% mortality, and cause two diseases: hemorrhagic fever with renal syndrome (HFRS) in Eurasia, and hantavirus cardiopulmonary syndrome (HCPS) in the Americas. Hantaviruses are enveloped and have a three-segmented, single-stranded, negative-sense RNA genome. The L gene encodes an RNA-dependent RNA polymerase, the M gene encodes two glycoproteins (Gn and Gc), and the S gene encodes a nucleocapsid protein. In addition, the S genes of some hantaviruses have an NSs open reading frame that can act as an interferon antagonist. Similarities between phylogenies have suggested ancient codivergence of the viruses and their hosts to many authors, but increasing evidence for frequent, recent host switching and local adaptation has led to questioning of this model. Infected rodents establish persistent infections with little or no effect on the host. Humans are infected from aerosols of rodent excreta, direct contact of broken skin or mucous membranes with infectious virus, or rodent bite. One hantavirus, Andes virus, is unique in that it is known to be transmitted from person-to-person. HFRS and HCPS, although primarily affecting kidneys and lungs, respectively, share a number of clinical features, such as capillary leakage, TNF-, and thrombocytopenia; notably, hemorrhages and alterations in renal function also occur in HCPS and cardiac and pulmonary involvement are not rare in HFRS. Of the four structural proteins, both in humoral and cellular immunity, the nucleocapsid protein appears to be the principal immunogen. Cytotoxic T-lymphocyte responses are seen in both HFRS and HCPS and may be important for both protective immunity and pathogenesis. Diagnosis is mainly based on detection of IgM antibodies although viral RNA (vRNA) may be readily, although not invariably, detected in blood, urine and saliva. For sero/genotyping neutralization tests/RNA sequencing are required. Formalin-inactivated vaccines have been widely used in China and Korea but not outside Asia. Hantaviruses are prime examples of emerging and re-emerging infections and, given the limited number of rodents and insectivores thus far studied, it is likely that many new hantaviruses will be detected in the near future.
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Book chapters on the topic "Protective antibodies"

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Bundle, David R., Casey Costello, Corwin Nycholat, Tomasz Lipinski, and Robert Rennie. "Designing a Candida albicans Conjugate Vaccine by Reverse Engineering Protective Monoclonal Antibodies." In Anticarbohydrate Antibodies, 121–45. Vienna: Springer Vienna, 2011. http://dx.doi.org/10.1007/978-3-7091-0870-3_5.

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Jennings, Harold J. "The Role of Sialic Acid in the Formation of Protective Conformational Bacterial Polysaccharide Epitopes." In Anticarbohydrate Antibodies, 55–73. Vienna: Springer Vienna, 2011. http://dx.doi.org/10.1007/978-3-7091-0870-3_3.

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Zabriskie, J. B., T. Poon-King, M. S. Blake, F. Michon, and M. Yoshinaga. "Phagocytic, Serological, and Protective Properties of Streptococcal Group A Carbohydrate Antibodies." In Streptococci and the Host, 917–19. Boston, MA: Springer US, 1997. http://dx.doi.org/10.1007/978-1-4899-1825-3_214.

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Jones, Trevor R., W. Ripley Ballou, and Stephen L. Hoffman. "Antibodies to the Circumsporozoite Protein and Protective Immunity to Malaria Sporozoites." In Progress in Clinical Parasitology, 103–17. New York, NY: Springer New York, 1993. http://dx.doi.org/10.1007/978-1-4612-2732-8_4.

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Van Regenmortel, Marc H. V. "Immune Systems Rather than Antigenic Epitopes Elicit and Produce Protective Antibodies Against HIV." In HIV/AIDS: Immunochemistry, Reductionism and Vaccine Design, 279–81. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-32459-9_22.

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Lukic, M. L., F. Y. Liew, and W. L. Chan. "Protective Effects of Monoclonal Antibodies and Immunopurified Glycoproteins in Primary HSV-1 Infection." In Microenvironments in the Lymphoid System, 855–61. Boston, MA: Springer US, 1985. http://dx.doi.org/10.1007/978-1-4613-2463-8_103.

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Neutra, Marian, Richard Weltzin, Louis Winner, Julie Mack, Pierre Michetti, Lynda Morrison, Bernard N. Fields, John J. Mekalanos, and Jean-Pierre Kraehenbuhl. "Identification and Use of Protective Monoclonal IgA Antibodies Against Viral and Bacterial Pathogens." In Advances in Experimental Medicine and Biology, 179–82. Boston, MA: Springer US, 1991. http://dx.doi.org/10.1007/978-1-4615-3838-7_22.

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Kamei, M., S. Hashizume, N. Sugimoto, Yue Ma, and M. Matsuda. "Anti-Tetanus Human Monoclonal Antibodies-Comparative Studies on Their Protective Activity with Polyclonal Antibody." In Animal Cell Technology: Basic & Applied Aspects, 521–25. Dordrecht: Springer Netherlands, 1992. http://dx.doi.org/10.1007/978-94-011-2844-5_70.

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Nakanaga, Kazue, Kazuya Yamanouchi, and Kosaku Fujiwara. "Protective Effect of the F(ab′)2 Fragments of Monoclonal Antibodies to Mouse Hepatitis Virus." In Coronaviruses, 365–71. Boston, MA: Springer US, 1987. http://dx.doi.org/10.1007/978-1-4684-1280-2_45.

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Mond, J. J., and J. F. Kokai-Kun. "The Multifunctional Role of Antibodies in the Protective Response to Bacterial T Cell-Independent Antigens." In Current Topics in Microbiology and Immunology, 17–40. Berlin, Heidelberg: Springer Berlin Heidelberg, 2008. http://dx.doi.org/10.1007/978-3-540-73900-5_2.

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Conference papers on the topic "Protective antibodies"

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Abo-Leyah, H., S. Gallant, D. Cassidy, Y. H. Giam, J. Killick, B. Marshall, G. Hay, et al. "The Seroprevalence and Protective Effect of SARS-COV-2 Antibodies in Scottish Healthcare Workers." In American Thoracic Society 2021 International Conference, May 14-19, 2021 - San Diego, CA. American Thoracic Society, 2021. http://dx.doi.org/10.1164/ajrccm-conference.2021.203.1_meetingabstracts.a1280.

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Hartweger, Harald, Mila Jankovic, and Michel C. Nussenzweig. "Abstract B113: Protective serum responses by CRISPR/Cas9-edited primary B cells expressing antibodies of choice." In Abstracts: Fourth CRI-CIMT-EATI-AACR International Cancer Immunotherapy Conference: Translating Science into Survival; September 30 - October 3, 2018; New York, NY. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/2326-6074.cricimteatiaacr18-b113.

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Marsolais, D., K. Walsh, B. Hahm, KH Edelmann, MB Oldstone, and H. Rosen. "Airway Delivery of a Sphingosine Analog Disrupts Antigen Presentation and Inhibits Virus-Specific CD8+T Cell Expansion While Sparing Generation of Protective Antibodies after Influenza Virus Infection." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a3252.

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Hartley, Adam, Michelle Williams, Amit Kaura, Mikhail Caga-Anan, Damini Dey, Marc Dweck, Dorian Haskard, David Newby, and Ramzi Khamis. "BS12 IgM and IgG anti-oxidised low-density lipoprotein antibodies predict protective atherosclerotic characterstics on cardiac ct: a substudy of the scottish computed tomography of the heart (SCOT-HEART) trial." In British Cardiovascular Society Virtual Annual Conference, ‘Cardiology and the Environment’, 7–10 June 2021. BMJ Publishing Group Ltd and British Cardiovascular Society, 2021. http://dx.doi.org/10.1136/heartjnl-2021-bcs.210.

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Koedam, Joost A., Rob J. Hamer, Nel H. Beeser-Visser, Etienne Jap Tjoen San, Kees Schippers, and Jan J. Sixma. "THE INTERACTION BETWEEN FACTOR VIII AND VON WILLEBRAND FACTOR." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644771.

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Factor VIII (FVIII) circulates in plasma as a non-covalent complex with von Willebrand factor (VWF), a large multimeric adhesive glycoprotein. VWF serves as a carrier for FVIII and is thought to stabilize FVIII. The interaction between the two proteins was studied by binding purified human 125I-FVIII to VWF which was coated on a solid matrix. Experiments employing isolated heavy and light chains of FVIII and monoclonal antibodies indicated that binding occurred through the carboxyterminal 80kDa light chain of factor VIII. Treatment of VWF-bound 125I-FVIII with thrombin resulted in the release of a light chain-derived 70kDa fragment and a heavy chain-derived 50kDa fragment. A 42kDa heavy chain-derived fragment was found in the fraction which remained bound to VWF. Treatment with factor Xa (FXa) resulted in the release of 63, 50, 45, and 42kDa fragments. No phospholipids were required for proteolysis of FVIII by either of these enzymes. In solution, the activation of FVIII by FXa, but not by thrombin, was inhibited by VWF. Neither activation, nor cleavage or release from VWF were observed when FVIII was incubated with factor IXa. Activation of FVIII was parallelled by its release from VWF. We conclude that the thrombin-activated form of FVIII consists of a complex between the 70kDa and 50kDa fragments. Inactivation of FVIII by activated protein C (APC) was inhibited when FVIII was complexed to VWF. This protective effect of VWF was abolished upon activation of FVIII and its subsequent release from VWF.In order to locate the binding site for FVIII on the VWF molecule, we digested VWF with Staphylococcal V8 protease (Sp). Digestion products were isolated with Mono Q ion-exchange chromatography and identified as Spl (39 kDa), SpII dimers (220 kDa) and Spill dimers (a triplet ranging from 210-280 kDa) by their molecular weight and chromatographic behaviour (J.-P. Girma et al.. Biochemistry 1986, 25:3156-3163). Purified VWF or digestion products were spotted on nitrocellulose paper, followed by blocking with an albumin solution. Binding of FVIII was studied by incubating the filters with 125I-FVIII, followed by autoradiography. Fifty ng of VWF was sufficient in order to detect FVIII binding. No binding was observed to partially reduced dimeric undigested VWF. Of the isolated digestion products, only the SpIII dimer was able to bind 125I-FVIII. After Western blotting of VWF-fragments from SDS-polyacrylamide gels, 125I-FVIII bound only to the bands which represented SpIII. Therefore, the domain on VWF responsible for the binding of FVIII seems to be located on its aminoterminal SpIII fragment. The integrity of internal disulfide bonds and dimerisation of VWF are required for FVIII binding.
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6

Thiagarajan, Divya, Nina Oparina, Johanna Steen, Mizanur Rahman, Max Vikström, Roman Zubarev, Susanna Lundström, and Johan Frostegård. "THU0216 IGG1 ANTIBODIES AGAINST PHOSPHORYLCHOLINE ARE ASSOCIATED WITH PROTECTION IN SLE AND ATHEROSCLEROSIS: POTENTIAL UNDERLYING MECHANISMS." In Annual European Congress of Rheumatology, EULAR 2019, Madrid, 12–15 June 2019. BMJ Publishing Group Ltd and European League Against Rheumatism, 2019. http://dx.doi.org/10.1136/annrheumdis-2019-eular.4169.

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7

Monaghan, TM, O. Negm, B. MacKenzie, M. Hamed, CC Shone, DP Humphreys, KR Acharya, and MH Wilcox. "PWE-017 High prevalence of subclass-specific binding and neutralising antibodies against clostridium difficile toxins in adult cystic fibrosis sera: possible mode of protection against symptomatic clostridium difficile infection." In British Society of Gastroenterology, Annual General Meeting, 19–22 June 2017, Abstracts. BMJ Publishing Group Ltd and British Society of Gastroenterology, 2017. http://dx.doi.org/10.1136/gutjnl-2017-314472.262.

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8

Clemens, R., G. Wirl, C. Velten, and H. J. Röthig. "VIRUS SAFETY OF ANTITHROMBIN III CONCENTRATE KYBERNIN P - APROSPECTIVE CLINICAL TRIAL." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644148.

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In 13 healthy male volunteers a prospective clinical trial was performed to evaluate virus safety of the antithrombin III concentrate Kybernin P in regard to hepatitis B, non-A/non-Band HIV transmission. As the volunteers were participants of a pharmacokinetic study they received either a fixed dosage of 1000 units Kybernin P asbolus injection or a dosage of 50 units per kg body weight as short-term infusion. Two different batches of Kybernin P were used.Whereas in all 13 volunteers virussafety in hepatitis non-A/non-B and HAV transmission could be monitored, only those volunteers who were not vaccinated (n=3) against hepatitis B or who had no protecting antibodies of anti-HB type despite vaccination (n=3)were to be included in the hepatitis B monitoring.All 13 volunteers were followed-upfor 1 year according to the standardsof the International Committee on Thrombosis and Hemostasis (ICTH). For detection of a potential hepatitis non-A/non-B transmission transaminases (AST, ALT) were determined in biweekly intervals during the first 6 months of the observation period and thereafter in monthly intervals. Hepatitis B seromar-kers as well as anti-HIV wereassessed bimonthly. Furthermore, all volunteers were clinically examined at every follow-up.None of the 13 volunteers revealedan increase of transaminases to the 2.5 fold of the upper normal level which is considered to be the borderlinelevel for hepatitis non-A/non-B diagnosis. Furthermore, in none of the volunteers a seroconversion for hepatitis B or HIV could be detected. Thus, Kybernin P is to be considered as hepatitis B, hepatitis non-A/non-B and HIV safe.
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9

Tokumaru, Kumon. "The Three Stage Digital Evolution of Linguistic Humans." In GLOCAL Conference on Asian Linguistic Anthropology 2019. The GLOCAL Unit, SOAS University of London, 2019. http://dx.doi.org/10.47298/cala2019.12-2.

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Digital Linguistics (DL) is an interdisciplinary study that identifies human language as a digital evolution of mammal analog vocal sign communications, founded on the vertebrate spinal sign reflex mechanism [Tokumaru 2017 a/b, 2018 a/b/c/d]. Analog signs are unique with their physical sound waveforms but limited in number, whilst human digital word signs are infinite by permutation of their logical property, phonemes. The first digital evolution took place 66,000 years ago with South African Neolithic industries, Howiesons Poort, when linguistic humans acquired a hypertrophied mandibular bone to house a descended larynx for vowel accented syllables containing logical properties of phonemes and morae. Morae made each syllable distinctive in the time axis and enabled grammatical modulation by alternately transmitting conceptual and grammatical syllables. The sign reflex mechanism is an unconscious self-protection and life-support mechanism, operated by immune cell networks inside the ventricle system. DL identified cellular and molecular structures for the sign (=concept) device as a B lymphocyte (or, in other words, Mobile Ad-Hoc Networking Neuron), connects to sensory, conceptual and networking memories, which consist of its meanings [Table 1]. Its antibodies can network with antigens of CSF-Contacting Neurons at the brainstem reticular formation and of Microglia cells at the neocortex [Figure 1]. It is plausible that the 3D structure of the antigen molecule takes the shape of word sound waveform multiplexing intensity and pitch, and that specifically pairing the antibody molecule consists of three CDRs (Complementality Defining Regions) in the Antibody Variable Region network with the logic of dichotomy and dualism. As sign reflex deals with survival issues such as food, safety and reproduction, it is stubborn, passive and inflexible: It does not spontaneously look for something new, and it is not designed to revise itself. These characteristics are not desirable for the development of human intelligence, and thus are to be overcome. All the word, sensory and network memories in the brain must be acquired postnatally through individual learning and thought. The reason and intelligence of humans depend on how correctly and efficiently humans learn new words and acquire appropriate meanings for them.
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Reports on the topic "Protective antibodies"

1

Jones, Trevor R., W. R. Ballou, and Stephen L. Hoffman. Antibodies to the Circumsporozoite Protein and Protective Immunity to Malaria Sporozoites. Fort Belvoir, VA: Defense Technical Information Center, January 1993. http://dx.doi.org/10.21236/ada266478.

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2

Cote, C. K., C. A. Rossi, A. S. Kang, P. R. Morrow, J. S. Lee, and S. L. Welkos. The Detection of Protective Antigen (PA) Associated with Spores of Bacillus Anthracis and the Effects of Anti-PA Antibodies on Spore Germination and Macrophage Interactions. Fort Belvoir, VA: Defense Technical Information Center, April 2005. http://dx.doi.org/10.21236/ada435638.

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