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Готові списки джерел за темами / Immunogenetics

Добірка наукової літератури з теми "Immunogenetics"

Автор: Grafiati

Опубліковано: 4 червня 2021

Оновлено: 6 вересня 2023

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Статті в журналах
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Книги
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Статті в журналах з теми "Immunogenetics":

1

Grennan, D. M. "Immunogenetics." Annals of the Rheumatic Diseases 44, no. 6 (June 1, 1985): 429. http://dx.doi.org/10.1136/ard.44.6.429-c.

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2

Steinmuller, David. "Immunogenetics." Mayo Clinic Proceedings 60, no. 4 (April 1985): 281. http://dx.doi.org/10.1016/s0025-6196(12)60324-3.

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3

Velosa, Jorge A. "Immunogenetics." Mayo Clinic Proceedings 60, no. 10 (October 1985): 721. http://dx.doi.org/10.1016/s0025-6196(12)60757-5.

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4

Wakeland, Edward K. "Immunogenetics." Current Opinion in Immunology 14, no. 5 (October 2002): 607–8. http://dx.doi.org/10.1016/s0952-7915(02)00391-6.

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5

Conley, Mary Ellen. "Immunogenetics." Current Opinion in Immunology 15, no. 5 (October 2003): 567–70. http://dx.doi.org/10.1016/s0952-7915(03)00106-7.

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6

Callard, R. "Immunogenetics." Journal of Immunological Methods 78, no. 1 (April 1985): 168–69. http://dx.doi.org/10.1016/0022-1759(85)90346-1.

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7

Alper, Chester A., and Charles E. Larsen. "Immunogenetics." Current Opinion in Immunology 16, no. 5 (October 2004): 623–25. http://dx.doi.org/10.1016/j.coi.2004.08.003.

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8

Wakeland, Edward K. "Immunogenetics." Current Opinion in Immunology 18, no. 5 (October 2006): 605–7. http://dx.doi.org/10.1016/j.coi.2006.07.018.

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9

Bender, K. "Immunogenetics." Experientia 42, no. 10 (October 1986): 1138–47. http://dx.doi.org/10.1007/bf01941288.

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10

Norman, Paul J. "Immunogenetics special issue 2023: Immunogenetics of infectious disease." Immunogenetics 75, no. 3 (May 23, 2023): 197–99. http://dx.doi.org/10.1007/s00251-023-01301-z.

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Дисертації з теми "Immunogenetics":

1

Middleton, D. "Histocompatibility and immunogenetics." Thesis, Queen's University Belfast, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.368778.

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2

Fanning, Gregory Charles. "Immunogenetics of systemic sclerosis." Thesis, University of Oxford, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.284535.

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3

Thomson, W. "Immunogenetics of rheumatoid arthritis." Thesis, University of Manchester, 1987. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.383908.

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4

Saini, Surinder Singh. "Molecular immunogenetics of bovine antibody." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape8/PQDD_0005/NQ40388.pdf.

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5

Anderson, Amy Elizabeth. "The immunogenetics of Helicobacter infection." Thesis, Imperial College London, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.414822.

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6

Ghosh, Soumitra. "Immunogenetics of Type I diabetes." Thesis, University of Oxford, 1992. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.306514.

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7

Else, Kathryn J. "Immunogenetics of Trichuris muris infection." Thesis, University of Nottingham, 1989. http://eprints.nottingham.ac.uk/12875/.

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Investigations have been made into the genetic control of immunity to the nematode Trichuris muris. Both background genes and genes within the mouse major histocompatibility complex (MHC), H-2, were shown to influence the expulsion of T. muris with the former having the stronger influence. At least two genes within the H-2 complex determined response phenotypes, the effects of "resistance" or "susceptibility" alleles at I-A being modulated by resistance or susceptibility alleles at aD end locus/loci. Differential responsiveness within slowly responding mouse strains suggested that parasite-dependent effects were also important. The primary antibody response to T. muris excretory/secretory (E/S) antigen, predominantly an IgG response, was also shown to be controlled by background and H-2-linked genes. In general, mouse strains less resistant to infection developed higher levels of IgG than- more resistant strains of mice. However strains of mice possessing the H-2q haplotype, irrespective of their genetic background, rapidly developed higher levels of IgG1 antibodies than strains of other haplotypes, H-2q haplotype mice tending to be more resistant to infection. Recognition of two high molecular weight (MW) E/S antigens by IgG as revealed by immunoprecipitation was also found to be almost exclusively H-2q restricted. This restriction may be partly quantitative but as such would operate in vivo due to the restriction on the ability to produce high levels of specific IgG. Both H-2q restricted phenomena may be part of, but not absolute requirements for, protective immunity. Parasite-induced effects on host immunity were also studied. Later larval and adult stages of T. muris were shown to be immunosuppressive, immunosuppression being long lasting and preventing the expulsion of subsequent infections. Vaccination with E/S antigen was shown to protect strains of mice which are slow to expel worms (poor-responder) or totally unable to expel worms (non-responder) from a primary infection with T. muris. However protection was slow to be expressed. Antigen recognition profiles of vaccinated strains of mice differed from their primary infection recognition profiles and included the recognition of the two high MW antigens shown to be H-2q restricted in a primary infection. Thus altering the mode or route of E/S antigen presentation may lead to shifts in responsiveness of H-2 genotypes to specific determinants and/or boost specific antibody levels sufficiently to reveal recognition of these antigens. Prior experience of a patent primary infection prevented vaccination protecting non-responder mice against subsequent infections. This inability was correlated with suppressed IgG1 antibody levels and failure to recognise three high MW antigens including the IL-2q restricted antigens. Using a panel of monoclonal antibodies raised against E/S antigen it was shown that E/S antigens, apparently including both immunogenic and immunosuppressive molecules, were localised to granules within the stichocyte cytoplasm of the adult T. muris stichosome.

8

Tozatto, Maio Karina. "Immunogenetics in sickle cell disease." Thesis, Sorbonne Paris Cité, 2019. http://www.theses.fr/2019USPCC093.

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La drépanocytose est l’hémoglobinopathie héréditaire la plus fréquente, causée par un polymorphisme unique d’un nucléotide (SNP) dans le gène de la beta-globine (HBB). Ce SNP détermine la synthèse de l’hémoglobine S, qui polymérise lorsqu’elle est soumise au stress, et ceci change la forme des hématies drépanocytaires en faucille. Les drépanocytes sont moins déformables, plus adhérents à l’endothélium, et plus susceptibles à l’hémolyse. Les complications cliniques de la drépanocytose peuvent être expliquées par l’interaction entre la vaso-occlusion, l’hémolyse et l’activation inflammatoire résultant de la présence des drépanocytes dans la circulation. Les patients drépanocytaires peuvent présenter de nombreuses complications, qui touchent tous les organes. La présentation clinique de cette maladie est très hétérogène, variant entre des patients qui ont très peu de symptômes à des patients qui décèdent de la maladie. Sachant que l’inflammation joue un rôle majeur dans la physiopathologie de la drépanocytose, des polymorphismes dans les gènes inflammatoires peuvent être évoqués pour expliquer cette hétérogénéité. La greffe de cellules souches hématopoïétiques est la seule thérapie curative disponible actuellement pour la drépanocytose, avec des bons résultats démontrés après la greffe d’un donneur apparenté HLA identique. Néanmoins, la plupart des patients n’a pas de donneur apparenté. Les patients drépanocytaires sont d’origine africaine, le groupe ethnique le moins représenté dans les registres de donneurs non apparentés de cellules souches. A ce jour, peu d’études, utilisant des registres locaux, ont été faites pour estimer la probabilité des patients drépanocytaires de trouver un donneur potentiel non apparenté dans les registres internationaux.Cette étude a eu pour objectif d’évaluer le rôle de quelques gènes inflammatoires liés aux Toll-like récepteurs (TLR) dans la survenue des infections bactériennes chez les patients drépanocytaires, vu que les infections sont une cause majeure de mortalité chez ces patients, et les TLR sont impliqués dans la reconnaissance de plusieurs types de bactéries. Les patients inclus avaient des échantillons d’ADN et des données cliniques disponibles. Les SNPs ont été génotypés par réaction en chaîne par polymérase en temps réel (RT-PCR). Quatre-cents trente patients, la plupart d’origine brésilienne ou africaine subsaharienne, ont été divisés en deux groupes : infectés (n=235, patients qui ont eu au moins un épisode d’infection bactérienne documentée) et non infectés (n=195, patients qui n’ont jamais présentés d’infections sévères). Le génotype T/A du SNP rs4696480 in TLR2 a été plus fréquent chez les patients non infectés (50% versus 67%, OR=0.50, 95% CI 0.34-0.75, p<0.001). En outre, le génotype T/T de ce SNP a été plus fréquent chez les patients infectés (15% versus 5%, OR=0.50, 95% CI 0.34-0.75, p<0.001). Des études précédentes ont démontré que les individus A/A avaient plus de sécrétion de marqueurs inflammatoires, lorsque l’allèle T était associé à moins de fréquence et de sévérité des maladies inflammatoires. Cette étude a également eu pour objectif d’estimer la probabilité de trouver un donneur potentiel non apparenté, antigène leucocytaire humain (HLA) allélique identique pour les loci HLA-A, HLA-B et HLA-DRB1. Dans cette étude, 185 patients ont été inclus, 116 suivis dans un centre brésilien et 69 greffés d’un donneur apparenté ou non apparenté dans des centres de greffe qui reportent leurs données à la Société Européenne de Greffe de Cellules Souches (EBMT). Les patients inclus avaient des données HLA testés en moyenne ou haute résolution. Les haplotypes HLA ont été estimés à travers un logiciel, HaploStats, et classifiés selon l’ethnicité. Ensuite, nous avons recherché des potentiels donneurs HLA alléliques identiques pour les loci HLA-A, HLA-B et HLA-DRB1 (6/6) dans des registres internationaux (WMDA)
Sickle cell disease (SCD) is the most common inherited hemoglobinopathy, caused by a single nucleotide polymorphism (SNP) in the beta-globin (HBB) gene. This SNP determines the synthesis of S haemoglobin (HbS), which polymerizes under stress conditions, sickling the red blood cell (RBC). Sickle RBC are less deformable, more adherent to the endothelium, and more susceptible to haemolysis. SCD complications are explained by the interaction between haemolysis, vaso-occlusion and inflammatory activation, determined by the RBC sickling. Patients with SCD may present several complications, affecting all organs. Clinical presentation is very heterogeneous, ranging from patients who have mild symptoms to patients who die from disease complications. Because inflammation plays a major role in SCD, polymorphisms in inflammatory genes are potential targets to explain this heterogeneity. Haematopoietic stem cell transplantation (HSCT) is the only curative therapy currently available for SCD, with good results shown after human leukocyte antigen (HLA) identical sibling HSCT. However, most patients will not have a matched sibling donor. Patients with SCD are mostly from African origin, the less represented ethnic group in stem cell donor registries. To date, few studies using local registries were performed to find the probability of having a potential unrelated donor in SCD settings. This study aimed to assess the role of inflammatory genes encoding Toll-like receptors (TLR) in the occurrence of bacterial infections in patients with SCD, because infection is a leading cause of mortality in SCD, and TLR recognize a wide range of bacteria. Patients included had DNA samples and clinical data available. SNPs were genotyped by real-time polymerase chain reaction (RT-PCR). Four hundred thirty patients, mostly from Brazilian and Sub-Saharan African origin, were divided in two groups: infected (n=235, patients who presented at least one episode of bacterial infection), and non-infected (n=195, patients who never presented bacterial infections). The T/A genotype of SNP rs4696480 in TLR2 was less frequent in infected patients (50% versus 67%, OR=0.50, 95% CI 0.34-0.75, p<0.001). In addition, the T/T genotype of this SNP was more frequent among infected patients (15% versus 5%, OR=0.50, 95% CI 0.34-0.75, p<0.001). Previous reports in other settings showed that A/A carriers had higher secretion of inflammatory markers, while T allele was associated with less occurrence and severity of inflammatory diseases. Hence, T/A genotype might express the ideal inflammatory response to defeat bacteria, while the weaker inflammatory response determined by the T/T genotype increases susceptibility to bacterial infections in SCD settings
A doença falciforme (DF) é a hemoglobinopatia hereditária mais frequente, causada por um polimorfismo de nucleotídeo único (SNP) no gene da betaglobina (HBB). A ocorrência desse SNP determina a síntese de hemoglobina S, que polimeriza sob condições de stress, alterando a conformação das hemácias, que adquirem forma de drepanócitos. Os drepanócitos são menos deformáveis, mais aderentes ao endotélio e mais suscetíveis à hemolise. As complicações clínicas da DF podem ser explicadas pela interação entre a vasoclusão, hemólise e ativação inflamatória resultantes da presença dos drepanócitos na circulação. Os pacientes com DF podem apresentar numerosas complicações, que afetam todos os órgãos. A apresentação clínica da DF é muito heterogênea, variando de pacientes pouco sintomáticos a pacientes que falecem por complicações da doença. Visto que a inflamação tem um papel importante na fisiopatologia da DF, polimorfismos em genes inflamatórios poderiam explicar essa heterogeneidade.O transplante de células tronco hematopoiéticas (TCPH) é a única terapia curativa disponível atualmente para a DF, com bons resultados demonstrados em TCPH de doador aparentado antígeno leucocitário humano (HLA) idêntico. Não obstante, a maioria dos pacientes não dispõe de doador aparentado HLA idêntico. A DF ocorre em pacientes normalmente de origem africana, o grupo étnico menos representado em registro de doadores de células tronco. Nos dias de hoje, poucos estudos, utilizando registros locais, avaliaram a probabilidade de encontrar potenciais doadores não aparentados para pacientes com DF. Este estudo teve por objetivo avaliar o papel de genes inflamaórios que codificam receptores Toll-like (TLR) na ocorrência de infecções bacterianas em pacientes com DF, visto que infecção é uma das principais causas de mortalidade em DF, e os TLR reconhecem diversos tipos de bactérias. Os pacientes incluídos no estudo tinham amostras de DNA e dados clínicos disponiveis. Os SNPs foram genotipados por reação em cadeia de polimerase em tempo real (RT-PCR). Quatrocentos e trinta pacientes, a maioria de orgem brasileira ou africana subsaariana, foram divididos em dois grupos, infectados (n=235, pacientes que apresentaram ao menos um episodio de infecção bacteriana), e não infectados (n=195, pacientes que nunca tiveram tais infecções). O genótipo T/A do SNP rs4696480 foi menos frequente em pacientes infectados (50% versus 67%, OR=0.50, 95% CI 0.34-0.75, p<0.001). Além disso, o genótipo T/T do mesmo SNP foi mais frequente em pacientes infectados (15% versus 5%, OR=0.50, 95% CI 0.34-0.75, p<0.001). Estudos prévios mostraram que indivíduos com genótipo A/A apresentavam mais secreção de marcadores inflamatórios, enquanto o alelo T foi associado a menor ocorrência e menor gravidade de doenças inflamatórias

9

Jeffery, Katherine Joanna Mary. "The immunogenetics of HTLV-I infection." Thesis, Imperial College London, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.392152.

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10

Goodman, Reyna Suzanne. "Immunogenetics of haematopoietic stem cell transplantation." Thesis, Anglia Ruskin University, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.478885.

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Книги з теми "Immunogenetics":

1

Christiansen, Frank T., and Brian D. Tait, eds. Immunogenetics. Totowa, NJ: Humana Press, 2012. http://dx.doi.org/10.1007/978-1-61779-842-9.

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2

O, McDevitt Hugh, ed. Immunogenetics. New York: Springer International, 1992.

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3

Williamson, Alan R. Essential immunogenetics. Oxford: Blackwell Scientific, 1987.

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4

Williamson, Alan R. Essential immunogenetics. Oxford: Blackwell Scientific Publications, 1987.

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5

Lesage, Sylvie. Immunogenetics: Tolerance and autoimmunity. Hauppauge, N.Y: Nova Science Publishers, 2010.

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6

Villanueva, Christian J. Immunogenicity. Hauppauge, N.Y: Nova Science, 2011.

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7

Bernal, J. E. Human immunogenetics: Principles and clinical applications. London: Taylor & Francis, 1986.

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8

Madrigal, Alejandro J., Margita Bencová, Derek Middleton, Dominique Charron, and Tibor Nánási, eds. Immunogenetics: Advances and Education. Dordrecht: Springer Netherlands, 1997. http://dx.doi.org/10.1007/978-94-011-5486-4.

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9

Carvalho, Agostinho, ed. Immunogenetics of Fungal Diseases. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-50842-9.

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10

R, Farid Nadir, ed. Immunogenetics of endocrine disorders. New York: Liss, 1988.

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Частини книг з теми "Immunogenetics":

1

Welsh, K. I. "Immunogenetics." In Immunotoxicity of Metals and Immunotoxicology, 37–41. Boston, MA: Springer US, 1990. http://dx.doi.org/10.1007/978-1-4684-8443-4_4.

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2

Lefranc, Marie-Paule. "Immunogenetics." In Encyclopedia of Systems Biology, 998. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4419-9863-7_259.

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3

Fleischhauer, Katharina, Peter A. Horn, and Andrea Harmer. "Immunogenetics Laboratory." In Establishing a Hematopoietic Stem Cell Transplantation Unit, 111–28. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-59358-6_8.

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4

Fuggle, Susan V., and Craig J. Taylor. "Histocompatibility and Immunogenetics." In Handbook of Renal and Pancreatic Transplantation, 55–75. Chichester, UK: John Wiley & Sons, Ltd, 2012. http://dx.doi.org/10.1002/9781118305294.ch4.

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5

Barnett, A. H. "Immunogenetics of Diabetes." In Immunology of Endocrine Diseases, 103–21. Dordrecht: Springer Netherlands, 1986. http://dx.doi.org/10.1007/978-94-009-4171-7_6.

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6

Hirbod-Mobarakeh, Armin, Mahsima Shabani, Mahsa Keshavarz-Fathi, Farnaz Delavari, Ali Akbar Amirzargar, Behrouz Nikbin, Anton Kutikhin, and Nima Rezaei. "Immunogenetics of Cancer." In Cancer Immunology, 417–78. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-30845-2_20.

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7

Amirzargar, Ali Akbar. "Immunogenetics of Aging." In Immunology of Aging, 219–29. Berlin, Heidelberg: Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-642-39495-9_16.

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8

Hirbod-Mobarakeh, Armin, Ali Akbar Amirzargar, Behrouz Nikbin, Mohammad Hossein Nicknam, Anton Kutikhin, and Nima Rezaei. "Immunogenetics of Cancer." In Cancer Immunology, 295–341. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-662-44006-3_17.

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9

Bach, Fritz H. "Immunogenetics of HLA." In Chronic Renal Disease, 529–35. Boston, MA: Springer US, 1985. http://dx.doi.org/10.1007/978-1-4684-4826-9_54.

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10

Burns, A., P. Li, and A. Rees. "Immunogenetics of Nephritis." In Immunology of Renal Disease, 1–28. Dordrecht: Springer Netherlands, 1991. http://dx.doi.org/10.1007/978-94-011-3902-1_1.

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Тези доповідей конференцій з теми "Immunogenetics":

1

Dehais and Mougenot. "An interactive system for database in immunogenetics." In Proceedings of the Twenty-Seventh Annual Hawaii International Conference on System Sciences. IEEE Comput. Soc. Press, 1994. http://dx.doi.org/10.1109/hicss.1994.323594.

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2

Williams, RMichael, and Edmond J. Yunis. "Abstract 2343: Immunogenetics of cancer and aging." 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.sabcs18-2343.

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3

Williams, RMichael, and Edmond J. Yunis. "Abstract 2343: Immunogenetics of cancer and aging." 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.am2019-2343.

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4

Refae, Sadal, Nathalie Ebran, Jocelyn Gal, Josiane Otto, Damien Giacchero, Delphine Borchiellini, Joel Guigay, Frederique Peyrade, Gerard Milano, and Esma Saada. "Abstract 4548: Host immunogenetics and hyperprogression under PD1/PD-L1 checkpoint inhibitors." In Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-4548.

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5

REFAE, Sadal, Jocelyn GAL, Nathalie EBRAN, Josiane OTTO, Delphine BORCHIELLINI, Frederic Peyrade, Emmanuel CHAMOREY, Patrick Brest, Gerard Alain Milano, and Esma SAADA-BOUZID. "Abstract 1370: Germinal immunogenetics predicts treatment outcome for PD1 PD-L1 checkpoint inhibitors." 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.sabcs18-1370.

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6

REFAE, Sadal, Jocelyn GAL, Nathalie EBRAN, Josiane OTTO, Delphine BORCHIELLINI, Frederic Peyrade, Emmanuel CHAMOREY, Patrick Brest, Gerard Alain Milano, and Esma SAADA-BOUZID. "Abstract 1370: Germinal immunogenetics predicts treatment outcome for PD1 PD-L1 checkpoint inhibitors." 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.am2019-1370.

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Levina, Julia, Leyla Namazova-Baranova, Kirill Savostyanov, Alexander Pushkov, Alexey Burdennyy, Anna Alekseeva, Kamilla Efendieva, and Elena Vishneva. "GP5 The immunogenetics and risk factors of pollinosis among russian children. case-control study." In Faculty of Paediatrics of the Royal College of Physicians of Ireland, 9th Europaediatrics Congress, 13–15 June, Dublin, Ireland 2019. BMJ Publishing Group Ltd and Royal College of Paediatrics and Child Health, 2019. http://dx.doi.org/10.1136/archdischild-2019-epa.72.

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8

Gu, Rong, and Hongyun Zhang. "The Application of Improved Immunogenetic Algorithm in Signal Timing." In 2009 International Joint Conference on Bioinformatics, Systems Biology and Intelligent Computing. IEEE, 2009. http://dx.doi.org/10.1109/ijcbs.2009.35.

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Gridina, S. L., V. F. Gridin, and O. I. Leshonok. "Characterization of High-Producing Cows by their Immunogenetic Status." In International scientific and practical conference "AgroSMART - Smart solutions for agriculture" (AgroSMART 2018). Paris, France: Atlantis Press, 2018. http://dx.doi.org/10.2991/agrosmart-18.2018.49.

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Ramonda, R., L. Punzi, A. Businaro, E. Musacchio, F. Schiavon, M. Podswiadek, G. Cardinale, and S. Todesco. "OP0050 Immunogenetic aspects of erosive osteoarthritis of the hand." In Annual European Congress of Rheumatology, Annals of the rheumatic diseases ARD July 2001. BMJ Publishing Group Ltd and European League Against Rheumatism, 2001. http://dx.doi.org/10.1136/annrheumdis-2001.417.

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Звіти організацій з теми "Immunogenetics":

1

Hutchinson, Mark, Janet Coller, Jillian Clark, Ruth Marshall, James Middleton, Vicky Staikopoulos, Melanie Gentgall, Francesca Alvaro, and Kathy Heyman. Chronic Pain Following Spinal Cord Injury: The Role of Immunogenetics and Time of Injury Pain Treatment. Fort Belvoir, VA: Defense Technical Information Center, October 2014. http://dx.doi.org/10.21236/ada613751.

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2

Hutchinson, Mark, Janet Coller, Jillian Clark, Ruth Marshall, James Middleton, Vicky Staikopoulos, Francesca Alvaro, and Kathy Heyman. Chronic Pain Following Spinal Cord Injury: The Role of Immunogenetics and Time of Injury Pain Treatment. Fort Belvoir, VA: Defense Technical Information Center, October 2012. http://dx.doi.org/10.21236/ada569291.

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3

Rodriguez, Jose E., Abebe T. Hassen, and James M. Reecy. Immunogenetic Factors Affecting Infectious Bovine Keratoconjuntivitis (IBK). Ames (Iowa): Iowa State University, January 2006. http://dx.doi.org/10.31274/ans_air-180814-476.

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4

David, Lior, Yaniv Palti, Moshe Kotler, Gideon Hulata, and Eric M. Hallerman. Genetic Basis of Cyprinid Herpes Virus-3 Resistance in Common Carp. United States Department of Agriculture, January 2011. http://dx.doi.org/10.32747/2011.7592645.bard.

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Анотація:

The goal of this project was to provide scientific and technical basis for initiating the development of breeding protocols using marker assisted selection for viral disease resistance in common carp. The specific objectives were: 1) Establishing families and characterizing the phenotypic and genetic variation of viral resistance; 2) Measuring the dynamics of immune response and developing a method to measure the long term immune memory; 3) Developing markers and generating a new genetic linkage map, which will enable initial QTL mapping; and, 4) Identifying genetic linkage of markers and candidate genes (like MHC and TLRs) with resistance to CyHV-3. The common carp is an important farmed freshwater fish species in the world. Edible carp is second only to tilapia in Israeli aquaculture production and ornamental carp (koi) is an important product in both the US and Israel. Carp industries worldwide have recently suffered enormous economic damage due to a viral disease caused by Cyprinid herpes virus 3 (CyHV-3). Aside from preventative measures, a sustainable solution to this problem will be to establish a genetic improvement program of the resistance of fish to the pathogen. The aims of the project was to take the necessary first steps towards that. The differences in survival rates after infection with CyHV-3 virus among 20 families from six types of crosses between three carp lines (two commercial lines and one wild-type carp) revealed that the wild-type carp and its crosses had a much-improved survival over the crosses of the commercial lines themselves. These crosses set the starting point for breeding of commercial strains with improved resistance. Resistant fish had lower antibody titer against the virus suggesting that resistance might depend more on the innate immunity. A set of 500 microsateliite markers was developed and the markers are currently being used for generating a genetic linkage map for carp and for identifying disease resistance QTL. Fourteen candidate immune genes, some of which were duplicated, were cloned from the carp and SNP markers were identified in them. The expression of these genes varied between tissues and suggested functional divergence of some duplicated genes. Initial association between CyHV-3 resistance and one of the genes was found when SNP alleles in these genes were tested for their segregation between susceptible and resistant progeny. The results of this project have implications to the development of viral resistant commercial carp strains and effective immunization against this aggressive disease. The genetic and immunological knowledge accumulated in this project will not only promote carp and koi production but will also contribute to a broader understanding of fish immunogenetics.