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Relevant bibliographies by topics / Antigen Presenting Cell

Academic literature on the topic 'Antigen Presenting Cell'

Author: Grafiati

Published: 4 June 2021

Last updated: 21 February 2023

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Journal articles on the topic "Antigen Presenting Cell"

1

Knight, Stella C., and Andrew J. Stagg. "Antigen-presenting cell types." Current Opinion in Immunology 5, no. 3 (June 1993): 374–82. http://dx.doi.org/10.1016/0952-7915(93)90056-x.

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Spillane, Katelyn M., and Pavel Tolar. "B cell antigen extraction is regulated by physical properties of antigen-presenting cells." Journal of Cell Biology 216, no. 1 (December 6, 2016): 217–30. http://dx.doi.org/10.1083/jcb.201607064.

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Antibody production and affinity maturation are driven by B cell extraction and internalization of antigen from immune synapses. However, the extraction mechanism remains poorly understood. Here we develop DNA-based nanosensors to interrogate two previously proposed mechanisms, enzymatic liberation and mechanical force. Using antigens presented by either artificial substrates or live cells, we show that B cells primarily use force-dependent extraction and resort to enzymatic liberation only if mechanical forces fail to retrieve antigen. The use of mechanical forces renders antigen extraction sensitive to the physical properties of the presenting cells. We show that follicular dendritic cells are stiff cells that promote strong B cell pulling forces and stringent affinity discrimination. In contrast, dendritic cells are soft and promote acquisition of low-affinity antigens through low forces. Thus, the mechanical properties of B cell synapses regulate antigen extraction, suggesting that distinct properties of presenting cells support different stages of B cell responses.

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Erb, P., M. Kennedy, P. Wassmer, and G. Huegli. "Antigen-presenting cells and T cell activation." Agents and Actions 19, no. 5-6 (December 1986): 266–68. http://dx.doi.org/10.1007/bf01971224.

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Gonnella, P. A., and D. W. Wilmore. "Co-localization of class II antigen and exogenous antigen in the rat enterocyte." Journal of Cell Science 106, no. 3 (November 1, 1993): 937–40. http://dx.doi.org/10.1242/jcs.106.3.937.

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The role of class II major histocompatibility antigens in classical antigen-presenting cells has been described (Unanue (1984) Annu. Rev. Immunol. 2, 395–428; Watts and McConnell (1987) Rev. Immunol. 5, 461–475). Whether enterocytes, which also express class II antigens, can act as antigen-presenting cells in vivo is not known. One pre-requisite for a role for enterocytes in antigen presentation is an interaction between exogenous antigen and class II antigens. Our results demonstrate that class II antigen and exogenous antigen absorbed from the gastrointestinal tract are co-localized within endocytic compartments and along the basolateral membranes of enterocytes.

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Fishman, Michael A., and Alan S. Perelson. "Modeling T Cell-Antigen Presenting Cell Interactions." Journal of Theoretical Biology 160, no. 3 (February 1993): 311–42. http://dx.doi.org/10.1006/jtbi.1993.1021.

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Horna, Pedro, Alex Cuenca, Fengdong Cheng, Jason Brayer, Hong-Wei Wang, Ivan Borrello, Hyam Levitsky, and Eduardo M. Sotomayor. "In vivo disruption of tolerogenic cross-presentation mechanisms uncovers an effective T-cell activation by B-cell lymphomas leading to antitumor immunity." Blood 107, no. 7 (April 1, 2006): 2871–78. http://dx.doi.org/10.1182/blood-2005-07-3014.

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AbstractBone marrow-derived antigen-presenting cells (APCs) play a central role in the induction of tolerance to tumor antigens expressed by B-cell lymphomas. Here we show that in vivo disruption of this APC-mediated tolerogenic mechanism unveils an intrinsic ability of malignant B cells to efficiently present tumor antigens to antigen-specific CD4+ T cells, resulting in a strong antitumor effect. This intrinsic antigen-presenting ability of malignant B cells is, however, overridden by tolerogenic bone marrow-derived APCs, leading instead to T-cell unresponsiveness and lack of antitumor effect. These results highlight the concept that therapeutic strategies aimed at enhancing the antigen-presenting function of B-cell lymphomas might not succeed unless the tolerogenic mechanisms mediated by bone marrow-derived APCs are disrupted in the first place.

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Raimondi, Giorgio, Ivan Zanoni, Stefania Citterio, Paola Ricciardi-Castagnoli, and Francesca Granucci. "Induction of Peripheral T Cell Tolerance by Antigen-Presenting B Cells. II. Chronic Antigen Presentation Overrules Antigen-Presenting B Cell Activation." Journal of Immunology 176, no. 7 (March 17, 2006): 4021–28. http://dx.doi.org/10.4049/jimmunol.176.7.4021.

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Apple, R. J., P. L. Domen, A. Muckerheide, and J. G. Michael. "Cationization of protein antigens. IV. Increased antigen uptake by antigen-presenting cells." Journal of Immunology 140, no. 10 (May 15, 1988): 3290–95. http://dx.doi.org/10.4049/jimmunol.140.10.3290.

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Abstract Cationization of BSA generates a molecule that mounts antibody responses of increased magnitude and duration and induces T cell proliferation at concentrations 500 times less than native BSA (nBSA). To explain the alteration in immunogenic properties of this Ag, the uptake of nBSA and cationized BSA (cBSA) by splenic APC has been investigated. T cell proliferation assays were conducted with nBSA and cBSA preparations with varying degrees of substitution. An inverse correlation between the degree of cationization and the amounts of Ag needed for optimal T cell reactivity was observed. To determine whether affinity for APC resulted in an increased uptake of cBSA, splenic APC were incubated with nBSA or cBSA for varying amounts of time. Comparisons were made at each time point between untreated Ag-pulsed APC (Ag uptake) and paraformaldehyde-fixed Ag-pulsed APC (processed Ag). Proliferation of T cells primed with nBSA or cBSA increased in proportion to the amount of time of APC exposure to high concentrations of nBSA, first appearing after a 2-h pulse and peaking at 8 h. Conversely, untreated APC needed only a 30-min cBSA exposure to induce either nBSA- or cBSA-primed T cell proliferation, indicating a rapid uptake of cBSA. Comparisons with proliferation induced by paraformaldehyde-fixed cBSA APC indicate that nBSA T cells recognize a lag phase-processed form of cBSA, whereas a majority of cBSA T cells recognize either a rapidly processed form of cBSA, or a membrane-processed cBSA molecule without a classical lag phase processing event. When monensin was used as an inhibitor of fluid phase pinocytosis in splenic APC, the presentation of nBSA was inhibited by 85%, but the presentation of cBSA was inhibited by only 20%. These results imply that nBSA enters the cell by fluid phase pinocytosis, whereas cBSA enters by a nonspecific adsorptive mechanism. The different modes of cellular entry for the two molecules, nBSA and cBSA, resulting in a rapid uptake of cBSA, may have important ramifications on T cell activation and immunoregulation.

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Lechler, R. I., M. A. Norcross, and R. N. Germain. "Qualitative and quantitative studies of antigen-presenting cell function by using I-A-expressing L cells." Journal of Immunology 135, no. 5 (November 1, 1985): 2914–22. http://dx.doi.org/10.4049/jimmunol.135.5.2914.

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Abstract I-A-expressing transfected murine L cells were analyzed as model antigen-presenting cells. Four features of accessory cell function were explored: antigen processing, interaction with accessory molecules (LFA-1, L3T4), influence of Ia density, and ability to stimulate resting, unprimed T lymphocytes. I-A+ L cells could present complex protein antigens to a variety of T cell hybridomas and clones. Paraformaldehyde fixation before but not subsequent to antigen exposure rendered I-A+ L cells unable to present intact antigen. These results are consistent with earlier studies that made use of these methods to inhibit "processing" by conventional antigen-presenting cells. The ability of anti-L3T4 antibody to inhibit T cell activation was the same for either B lymphoma or L cell antigen-presenting cells. In striking contrast, anti-LFA-1 antibody, which totally blocked B lymphoma-induced responses, had no effect on L cell antigen presentation, measured as interleukin 2 (IL 2) release by T hybridomas, proliferation, IL 2 release, or IL 2 receptor upregulation by a T cell clone. I-A+ L cell transfectants were found to have a stable level of membrane I-A and I-A mRNA, even after exposure to interferon-gamma-containing T cell supernatants. In agreement with earlier reports, a proportional relationship between the (Ia) X (Ag) product and T cell response was found for medium or bright I-A+ cells. However, dull I-A+ cells had a disproportionately low stimulatory capacity, suggesting that there may be a threshold density of Ia per antigen-presenting cell necessary for effective T cell stimulation. Finally, I-A-bearing L cells were shown to trigger low, but reproducible primary allogeneic mixed lymphocyte responses with the use of purified responder T cells, indicating that they are capable of triggering even resting T cells. These studies confirm the importance of antigen processing and I-A density in antigen-presenting cell function, but raise questions about the postulated role of the LFA-1 accessory molecule in T cell-antigen-presenting cell interaction. They also illustrate the utility of the L cell transfection model for analysis and dissection of antigen-presenting cell function.

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Rossjohn, Jamie, Stephanie Gras, John J. Miles, Stephen J. Turner, Dale I. Godfrey, and James McCluskey. "T Cell Antigen Receptor Recognition of Antigen-Presenting Molecules." Annual Review of Immunology 33, no. 1 (March 21, 2015): 169–200. http://dx.doi.org/10.1146/annurev-immunol-032414-112334.

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Dissertations / Theses on the topic "Antigen Presenting Cell"

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Chang, Nan-Hua. "Selective elimination of antigen-specific T cells by antigen-targeted drug-labeled antigen-presenting cell membranes." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp02/NQ27889.pdf.

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Hudson, Sarah. "Myeloid antigen presenting cell populations in the murine uterus /." Title page, abstract and contents only, 2000. http://web4.library.adelaide.edu.au/theses/09PH/09phh887.pdf.

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Fidler, Sarah. "Antigen presenting cell function in HIV-1 infection." Thesis, Imperial College London, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.300156.

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Dorrell, Lucy. "Antigen-presenting cell function in HIV infection and tuberculosis." Thesis, University of Southampton, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.241984.

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Wyss-Coray, Anton. "The human T lymphocyte as an antigen presenting cell /." [S.l : s.n.], 1993. http://www.ub.unibe.ch/content/bibliotheken_sammlungen/sondersammlungen/dissen_bestellformular/index_ger.html.

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Bergamin, Fabio. "Antigen-presenting cells and BAFF in porcine B-cell responses against FMDV /." Bern : [s.n.], 2007. http://www.ub.unibe.ch/content/bibliotheken_sammlungen/sondersammlungen/dissen_bestellformular/index_ger.html.

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Pecora, Nicole Danielle. "TLR₂-dependent modulation of antigen presenting cell functions by mycobacterial lipoproteins." Cleveland, Ohio : Case Western Reserve University, 2008. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=case1212611434.

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Giusti, Pablo. "Characterization of antigen-presenting cell function in vitro and ex vivo." Doctoral thesis, Stockholms universitet, Wenner-Grens institut, 2011. http://urn.kb.se/resolve?urn=urn:nbn:se:su:diva-60433.

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Long-term protective immunity depends on proper initiation of professional antigen-presenting cells (APCs). Autoimmune disorders and certain infections can cause disease through modulation of APCs and thereby affecting the outcome of these diseases. This work aimed to investigate the behaviour of different APC subsets during conditions known to cause improper immune responses. In Paper I, the effects of an anti-inflammatory compound called Rabeximod, intended for treatment of rheumatoid arthritis were investigated on different subsets of APCs. The results showed that Rabeximod affected the differentiation and behaviour of inflammatory subsets of dendritic cells (DCs) and macrophages while no effects were observed on anti-inflammatory subsets. Our findings suggest that Rabeximod acts by inhibiting the functionality of inflammatory subsets of APCs. In Paper II, the effects of different malaria derived stimuli such as hemozoin (Hz) and infected red-blood cells (iRBCs) on monocyte-derived dendritic cells (MoDCs) were investigated. Both stimuli triggered activation and migration of MoDCs. MoDCs exposed to iRBCs induced allogeneic T-cell proliferation while those exposed to Hz did not. These results indicate that different malaria derived stimuli may differently affect DCs and that this could lead to improper and inefficient T-cell activation. In Paper III, innate aspects of malarial immunity were compared in children from two sympatric ethnic groups. We observed decreased activation of APCs and severely supressed TLR responses in Dogon children as compared to Fulani. This may indicate an important role for TLR and APC activation in the Fulani, known to be better protected against malaria than the Dogon. In summary, detailed knowledge of APC activation will be helpful in the understanding of specific effector immune responses. This could in turn, improve treatment of inflammatory disorders as well as the generation of efficient vaccines against infectious diseases.

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Pecora, Nicole Danielle. "TLR2-Dependent Modulation of Antigen Presenting Cell Functions by Mycobacterial Lipoproteins." Case Western Reserve University School of Graduate Studies / OhioLINK, 2008. http://rave.ohiolink.edu/etdc/view?acc_num=case1212611434.

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Mayer, Wolfgang. "The antigen presenting cell in the human cornea – functional and morphological evaluation." Diss., lmu, 2012. http://nbn-resolving.de/urn:nbn:de:bvb:19-143669.

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Books on the topic "Antigen Presenting Cell"

1

Harald, Kropshofer, and Vogt Anne B, eds. Antigen presenting cells: From mechanisms to drug development. Weinheim: Wiley-VCH, 2005.

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2

Chang, Nan-Hua. Selective elimination of antigen-specific T cells by antigen-targeted drug-labeled antigen-presenting cell membranes. Ottawa: National Library of Canada = Bibliothèque nationale du Canada, 1997.

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3

Z, Atassi M., and Abbott Laboratories, eds. Immunobiology of proteins and peptides IV: T-cell recognition and antigen presentation. New York: Plenum Press, 1987.

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4

Antigen-presenting cells. Oxford: IRL Press at Oxford University Press, 1989.

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5

Benvenuto, Pernis, Silverstein Samuel C, and Vogel Henry J. 1920-, eds. Processing and presentation of antigens. San Diego: Academic Press, 1988.

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6

James, McCluskey, ed. Antigen processing and recognition. Boca Raton: CRC Press, 1991.

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1953-, Angelov D. N., ed. The cerebral perivascular cells. Berlin: Springer, 1998.

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Edward, Humphreys Robert, and Pierce Susan K, eds. Antigen processing and presentation. San Diego: Academic Press, 1994.

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9

Kang, Chʻang-yul. Pairŏsŭ pektʻŏ ro hyŏngjil toiptoen hangwŏn chesi sepʻo ŭi myŏnyŏk chʻiryoje yuhyosŏng pʻyŏngka mit sihŏmpŏp yŏnʼgu =: Development and estimation of immunotherapeutic cell-based vaccine approaches using antigen presenting cells transduced with viral vector. [Seoul]: Sikpʻum Ŭiyakpʻum Anjŏnchʻŏng, 2007.

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10

Viner, Nicholas John. Antigen presenting cells in inflammatory arthritis. Birmingham: University of Birmingham, 1992.

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Book chapters on the topic "Antigen Presenting Cell"

1

Lebedeva, Tatiana, Michael L. Dustin, and Yuri Sykulev. "Target Cell Contributions to Cytotoxic T Cell Sensitivity." In Antigen Presenting Cells, 199–220. Weinheim, FRG: Wiley-VCH Verlag GmbH & Co. KGaA, 2006. http://dx.doi.org/10.1002/3527607021.ch7.

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Havenith, Carin E. G., Annette J. Breedijk, Wim Calame, Robert H. J. Beelen, and Elisabeth C. M. Hoefsmit. "Antigen Specific T Cell Priming in Vivo by Intratracheal Injection of Antigen Presenting Cells." In Advances in Experimental Medicine and Biology, 571–75. Boston, MA: Springer US, 1993. http://dx.doi.org/10.1007/978-1-4615-2930-9_95.

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Wilke, Cailin Moira, Shuang Wei, Lin Wang, Ilona Kryczek, Jingyuan Fang, Guobin Wang, and Weiping Zou. "T Cell and Antigen-Presenting Cell Subsets in the Tumor Microenvironment." In Cancer Immunotherapy, 17–44. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4614-4732-0_2.

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Izon, David J., John D. Nieland, Lori A. Jones, and Ada M. Kruisbeek. "T Cell Tolerance and Antigen Presenting Cell Function in the Thymus." In Advances in Experimental Medicine and Biology, 159–64. Boston, MA: Springer US, 1993. http://dx.doi.org/10.1007/978-1-4615-2930-9_27.

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De Becker, Geneviève, Philippe Mockel, Jacques Urbain, Oberdan Leo, and Muriel Moser. "Enhanced Antigen Presenting Cell Function Following in Vivo Priming." In Advances in Experimental Medicine and Biology, 189–93. Boston, MA: Springer US, 1997. http://dx.doi.org/10.1007/978-1-4757-9966-8_32.

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Platzman, Ilia, Gerri Kannenberg, Jan-Willi Janiesch, Jovana Matić, and Joachim P. Spatz. "PEG-Based Antigen-Presenting Cell Surrogates for Immunological Applications." In Soft Matter Nanotechnology, 187–216. Weinheim, Germany: Wiley-VCH Verlag GmbH & Co. KGaA, 2015. http://dx.doi.org/10.1002/9783527682157.ch07.

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Romieu-Mourez, Raphaëlle, and Jacques Galipeau. "Mesenchymal Stromal Cells as Effective Tumor Antigen-Presenting Cells in Cancer Therapeutics." In Stem Cell Therapeutics for Cancer, 127–43. Hoboken, NJ: John Wiley & Sons, Inc, 2013. http://dx.doi.org/10.1002/9781118660423.ch10.

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Pierce, Susan K., Ellen K. Lakey, Emanuel Margoliash, Lori A. Smolenski, and Lisa A. Casten. "The Presentation of Processed, Ia Restricted, T Cell Antigenic Peptides on Antigen Presenting Cell Surfaces." In H-2 Antigens, 485–92. Boston, MA: Springer US, 1987. http://dx.doi.org/10.1007/978-1-4757-0764-9_48.

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Jenkins, Marc K., Dimuthu R. DeSilva, Julia G. Johnson, and Steven D. Norton. "Costimulating Factors and Signals Relevant for Antigen Presenting Cell Function." In Advances in Experimental Medicine and Biology, 87–92. Boston, MA: Springer US, 1993. http://dx.doi.org/10.1007/978-1-4615-2930-9_15.

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Alaoui, Lamine, Mélanie Durand, and Elodie Segura. "Identification of Antigen Presenting Cell Subsets Supporting Human Tfh Differentiation." In Methods in Molecular Biology, 125–39. New York, NY: Springer US, 2021. http://dx.doi.org/10.1007/978-1-0716-1736-6_11.

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Conference papers on the topic "Antigen Presenting Cell"

1

Perica, Karlo, Joan G. Bieler, Andrés De León Medero, Yen-Ling Chiu, Malarvizhi Durai, Michaela Niemöller, Mario Assenmacher, Anne Richter, Mathias Oelke, and Jonathan Schneck. "Abstract 4531: Nanoscale Artificial Antigen Presenting Cells for T Cell Immunotherapy." 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.am2013-4531.

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Kedmi, Ranit, Kai Mesa, and Dan Littman. "Abstract B167: Antigen-presenting cells as coordinators of T-cell responses to gut microbiota." 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-b167.

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Schneiders, Famke L., Saskia J. A. M. Santegoets, Rik J. Scheper, Henk M. W. Verheul, Marc Bonneville, Emmanuel Scotet, Tanja D. de Gruijl, and Hans J. van der Vliet. "Abstract 3533: Acquisition of antigen presenting cell functions by Vγ9Vα2-T cells requires trogocytosis." 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.am2012-3533.

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Xu, Yaqin, Anja Krause, Tilla Worgall, Maria Limberis, and Stefan Worgall. "Impaired T Cell Stimulation And Lipid Antigen Presentation By Pulmonary, But Not Systemic, CD11c+ Antigen-Presenting Cells In Cystic Fibrosis." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a2447.

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Zhang, David K. Y., Anna Vaynrub, and David J. Mooney. "Abstract B058: Rapid and controlled T-cell expansion using scaffolds that mimic antigen-presenting cells." 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-b058.

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McLaughlin, Ryan, and Mario Perhinschi. "Abnormal Condition Identification Using Antigen Presenting Cell Approach for a Partitioned Immune System." In AIAA SCITECH 2023 Forum. Reston, Virginia: American Institute of Aeronautics and Astronautics, 2023. http://dx.doi.org/10.2514/6.2023-1659.

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Zhang, Xuqing, Shamael R. Dastagir, Naren Subbiah, Mengyao Luo, Vikram Soman, Sneha Pawar, Douglas C. McLaughlin, et al. "Abstract 3260: Engineered red-cell therapeutics (RCT) as artificial antigen presenting cells promotein vivoexpansion and anti-tumor activity of antigen specific T cells." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.am2019-3260.

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Zhang, Xuqing, Shamael R. Dastagir, Naren Subbiah, Mengyao Luo, Vikram Soman, Sneha Pawar, Douglas C. McLaughlin, et al. "Abstract 3260: Engineered red-cell therapeutics (RCT) as artificial antigen presenting cells promotein vivoexpansion and anti-tumor activity of antigen specific T cells." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-3260.

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von Garnier, Christophe, Deborah Strickland, Philip Stumbles, Patrick G. Holt, and Fabian Blank. "Size Determines Particle Uptake Efficiency And Trafficking By Prominent Respiratory Tract Antigen Presenting Cell Populations." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a2245.

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Jansen, Caroline S., Nataliya Prokhnevska, Viraj A. Master, Jennifer W. Carlisle, Mehmet A. Bilen, Adriana M. Reyes, and Haydn T. Kissick. "Abstract 2700: CD8 T-cell infiltration into renal tumors requires a supportive antigen-presenting niche." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-2700.

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Reports on the topic "Antigen Presenting Cell"

1

Schneck, Jonathan P., and Mathias Oelke. Development of Artificial Antigen Presenting Cells for Prostate Cancer Immunotherapy. Fort Belvoir, VA: Defense Technical Information Center, May 2005. http://dx.doi.org/10.21236/ada456218.

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Schneck, Jonathan P., and Mathis Oelke. Development of Artificial Antigen Presenting Cells for Prostate Cancer Immunotherapy. Fort Belvoir, VA: Defense Technical Information Center, May 2004. http://dx.doi.org/10.21236/ada429835.

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Schneck, Jonathan P., and Mathias Oelke. Development of Artificial Antigen Presenting Cells for Prostate Cancer Immunotherapy. Fort Belvoir, VA: Defense Technical Information Center, May 2007. http://dx.doi.org/10.21236/ada482123.

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Oelke, Mathias. Development of Antigen Presenting Cells for Adoptive Immunotherapy in Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, December 2006. http://dx.doi.org/10.21236/ada466160.

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Oelke, Mathias. Development of Antigen Presenting Cells for Adoptive Immunotherapy in Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, December 2007. http://dx.doi.org/10.21236/ada482669.

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Malkinson, Mertyn, Irit Davidson, Moshe Kotler, and Richard L. Witter. Epidemiology of Avian Leukosis Virus-subtype J Infection in Broiler Breeder Flocks of Poultry and its Eradication from Pedigree Breeding Stock. United States Department of Agriculture, March 2003. http://dx.doi.org/10.32747/2003.7586459.bard.

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Objectives 1. Establish diagnostic procedures to identify tolerant carrier birds based on a) Isolation of ALV-J from blood, b) Detection of group-specific antigen in cloacal swabs and egg albumen. Application of these procedures to broiler breeder flocks with the purpose of removing virus positive birds from the breeding program. 2. Survey the AL V-J infection status of foundation lines to estimate the feasibility of the eradication program 3. Investigate virus transmission through the embryonated egg (vertical) and between chicks in the early post-hatch period (horizontal). Establish a model for limiting horizontal spread by analyzing parameters operative in the hatchery and brooder house. 4. Compare the pathogenicity of AL V-J isolates for broiler chickens. 5. Determine whether AL V-J poses a human health hazard by examining its replication in mammalian and human cells. Revisions. The: eradication objective had to be terminated in the second year following the closing down of the Poultry Breeders Union (PBU) in Israel. This meant that their foundation flocks ceased to be available for selection. Instead, the following topics were investigated: a) Comparison of commercial breeding flocks with and without myeloid leukosis (matched controls) for viremia and serum antibody levels. b) Pathogenicity of Israeli isolates for turkey poults. c) Improvement of a diagnostic ELISA kit for measuring ALV-J antibodies Background. ALV-J, a novel subgroup of the avian leukosis virus family, was first isolated in 1988 from broiler breeders presenting myeloid leukosis (ML). The extent of its spread among commercial breeding flocks was not appreciated until the disease appeared in the USA in 1994 when it affected several major breeding companies almost simultaneously. In Israel, ML was diagnosed in 1996 and was traced to grandparent flocks imported in 1994-5, and by 1997-8, ML was present in one third of the commercial breeding flocks It was then realized that ALV-J transmission was following a similar pattern to that of other exogenous ALVs but because of its unusual genetic composition, the virus was able to establish an extended tolerant state in infected birds. Although losses from ML in affected flocks were somewhat higher than normal, both immunosuppression and depressed growth rates were encountered in affected broiler flocks and affected their profitability. Conclusions. As a result of the contraction in the number of international primary broiler breeders and exchange of male and female lines among them, ALV-J contamination of broiler breeder flocks affected the broiler industry worldwide within a short time span. The Israeli national breeding company (PBU) played out this scenario and presented us with an opportunity to apply existing information to contain the virus. This BARD project, based on the Israeli experience and with the aid of the ADOL collaborative effort, has managed to offer solutions for identifying and eliminating infected birds based on exhaustive virological and serological tests. The analysis of factors that determine the efficiency of horizontal transmission of virus in the hatchery resulted in the workable solution of raising young chicks in small groups through the brooder period. These results were made available to primary breeders as a strategy for reducing viral transmission. Based on phylogenetic analysis of selected Israeli ALV-J isolates, these could be divided into two groups that reflected the countries of origin of the grandparent stock. Implications. The availability of a simple and reliable means of screening day old chicks for vertical transmission is highly desirable in countries that rely on imported breeding stock for their broiler industry. The possibility that AL V-J may be transmitted to human consumers of broiler meat was discounted experimentally.

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