Avian Models of Autoimmune Disease: Lessons from the Birds

Rose, Noel R.

doi:10.3382/ps.0730984

Cited by 23 publications

(11 citation statements)

References 20 publications

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“…A comprehensive review on the MHC linkage with differences in disease resistance has been given in several papers: resistance to viral infections [18,42,66,88,104,133,137], resistance to bacterial infections [29,46,122], resistance to protozoal infection [21,86,129], and autoimmune diseases [114].…”

Section: Definition Mhc and Disease Resistancementioning

confidence: 99%

Immunological basis of differences in disease resistance in the chicken

Zekarias

Huurne²,

Landman

et al. 2002

Vet. Res.

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-Genetic resistance to diseases is a multigenic trait governed mainly by the immune system and its interactions with many physiologic and environmental factors. In the adaptive immunity, T cell and B cell responses, the specific recognition of antigens and interactions between antigen presenting cells, T cells and B cells are crucial. It occurs through a network of mediator proteins such as the molecules of the major histocompatibility complex (MHC), T cell receptors, immunoglobulins and secreted proteins such as the cytokines and antibodies. The diversity of these proteins that mainly is due to an intrinsic polymorphism of the genes causes phenotypic variation in disease resistance. The well-known linkage of MHC polymorphism and Marek's disease resistance difference represents a classic model revealing immunological factors in resistance differences and diversity of mediator molecules. The molecular bases in any resistance variation to infectious pathogens are vaguely understood. This paper presents a review of the major immune mediators involved in resistance and susceptibility to infectious diseases and their functional mechanisms in the chicken. The genetic interaction of disease resistance with production traits and the environment is mentioned. et les interactions entre les cellules présentant des antigènes, les cellules T et B, sont cruciales. Cela se produit à travers un réseau de protéines médiatrices telles que les molécules du complexe majeur d'histocompatibilité (CMH), les récepteurs des cellules T, les immunoglobulines et les protéines sé-crétées telles que les cytokines et les anticorps. La diversité de ces protéines, qui est surtout due au polymorphisme intrinsèque des gènes, entraîne une variation phénotypique dans la résistance aux maladies. Le lien bien connu entre le polymorphisme du CMH et les différences dans la résistance à la maladie de Marek représente un modèle classique révélant les facteurs immunologiques dans les différences de résistance et la diversité dans les molécules médiatrices. Les bases moléculaires impliquées dans toute variation de résistance aux pathogènes infectieux sont à peu près comprises. Cet article présente une synthèse sur les principaux médiateurs de l'immunité impliqués dans la résis-tance et la sensibilité aux maladies infectieuses chez le poulet et leurs mécanismes fonctionnels. L'interaction génétique entre la résistance aux maladies et les traits de production et l'environnement est mentionnée.

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Section: Definition Mhc and Disease Resistancementioning

confidence: 99%

Immunological basis of differences in disease resistance in the chicken

Zekarias

Huurne²,

Landman

et al. 2002

Vet. Res.

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“…Animal models have historically complemented the discovery of disease etiology and progression by making it possible to examine events that are difficult to study in humans [27][28][29]. The egg-laying hen is the only spontaneous model of ovarian cancer.…”

Section: Introductionmentioning

confidence: 99%

Selenium-Binding Protein 1 expression in ovaries and ovarian tumors in the laying hen, a spontaneous model of human ovarian cancer

Stammer

Edassery

Barua

et al. 2008

Gynecologic Oncology

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Objective-Reduced Selenium-Binding Protein 1 (SELENBP1) expression was recently shown in multiple cancers. There is little information on the expression and function of SELENBP1 in cancer progression. In order to develop a better understanding of the role of SELENBP1 in ovarian cancer, our objective was to determine if SELENBP1 is expressed in the normal ovaries and ovarian tumors in the egg-laying hen, a spontaneous model of human ovarian cancer.Methods-SPB1 mRNA expression in normal ovary (n=20) and ovarian tumors (n=23) was evaluated by RT-PCR. Relative levels of mRNA were compared by quantitative RT-PCR (qRT-PCR) in selected samples. SELENBP1 protein expression was evaluated by 1D Western Blot and immunohistochemistry with a commercial anti-human SELENBP1 antibody.Results-SELENBP1 mRNA and protein was expressed in 100% of normal and ovarian tumors and qRT-PCR confirmed decreased mRNA expression in 80% of ovarian tumors. SELENBP1 was primarily localized in surface epithelial cells of normal ovaries. In ovaries containing early tumor lesions, SELENBP1 expression was reduced in the surface epithelium near the tumor and was expressed in tumor cells, while more distant regions with normal histology retained SELENBP1 expression in the surface epithelium.Conclusions-We have shown for the first time that SELENBP1 is expressed in both normal ovaries and ovarian tumors in the hen and that SELENBP1 expression is altered in the vicinity of the tumor. Furthermore, SELENBP1 expression in normal ovarian surface epithelium and in ovarian tumors parallels that previously reported for ovarian cancer in women.

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“…Different types of rodents, 5 nonhuman primates, 6 and avian models 7,8 have been also used in MS research, which has enriched our insight into different pathologic aspects of MS. The commonly studied major categories of rodent models are the EAE model, the virally induced (e.g., TMEV) infection chronic demyelinating models, toxin (e.g., cuprizone and lysophosphatidyl choline-induced demyelination) models, 5,9 and the genetically altered mouse.…”

Section: Discussionmentioning

confidence: 99%

“…It is expected, given the complex nature of the disease and its multifactorial etiology, that a single animal model will not provide insight into all clinical, radiologic, pathologic, and genetic features of MS. In addition to frequently used rodent models, 5 nonhuman primates 6 and avian models 7,8 are used in MS research, which has expanded our understanding of different pathologic aspects of MS. The most commonly studied major categories of animal/ rodent models of MS include experimental autoimmune encephalomyelitis (EAE), virally induced (e.g., Theiler's murine encephalomyelitis virus [TMEV] infection) chronic demyelinating models, and toxin-induced models of demyelination such as the cuprizone and focal demyelination induced by lysophosphatidyl choline models.…”

mentioning

confidence: 99%