Zobrazeno 1 - 10
of 75
pro vyhledávání: '"N, Brenden"'
Publikováno v:
Scandinavian Journal of Immunology. 57:342-349
The nonobese diabetic (NOD) mouse is a useful model for human autoimmune diabetes. The gene for the anti-apoptotic protein Bcl-2 has previously been suggested as a probable susceptibility candidate for the NOD mouse disease. In this study, we investi
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::6463f5586503c979ed15904bce3c0266
https://doi.org/10.1046/j.1365-3083.2003.01244.x
https://doi.org/10.1046/j.1365-3083.2003.01244.x
Publikováno v:
Scandinavian Journal of Immunology. 54:470-476
The nonobese diabetic (NOD) mouse model is a model of human autoimmune insulin dependent diabetes, IDDM. The effector cells of the disease have been shown to be T cells, but also B cells seem to contribute. Adult NOD mice have been shown to display a
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_________::46c57264ab9e496ece1b2ec62bbca749
https://doi.org/10.1046/j.1365-3083.2001.00991.x
https://doi.org/10.1046/j.1365-3083.2001.00991.x
Publikováno v:
Scandinavian Journal of Immunology. 50:405-410
The E complex of the major histocompatibility complex (MHC) can prevent the spontaneous development of diabetes in nonobese diabetic (NOD) mice transgenic for the Ea gene. None of three promoter-mutated Ea constructs with Ea expression directed to di
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::22cb9fa0b3f73a2cc9a304371a10e23d
https://doi.org/10.1046/j.1365-3083.1999.00613.x
https://doi.org/10.1046/j.1365-3083.1999.00613.x
Autor:
Jan Böhme, N. Brenden
Publikováno v:
Immunogenetics. 49:1-6
Positive selection has been proposed to be involved in protection from diabetes. We examined positive selection by fluorescence-activated cell sorter analyses in thymocytes of protected and susceptible E-transgenic and non-transgenic NOD mice. Three
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::e698e85d5ebc9ce73610e011345aa613
https://doi.org/10.1007/s002510050457
https://doi.org/10.1007/s002510050457
No Evidence for TCR Vbeta Repertoire Changes Influencing Disease Protection in E-Transgenic NOD Mice
Publikováno v:
Scandinavian Journal of Immunology. 42:135-139
In order to study whether positive selection of T cells plays any role in the MHC-dependent protection from diabetes in the non-obese-diabetic (NOD) mouse, the T cell V beta repertoire has been studied in NOD mice and in NOD mice either transgenic fo
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::d158936a0ed93dac6eaf971381c0323b
https://doi.org/10.1111/j.1365-3083.1995.tb03636.x
https://doi.org/10.1111/j.1365-3083.1995.tb03636.x
Publikováno v:
Scandinavian journal of immunology. 54(5)
The nonobese diabetic (NOD) mouse model is a model of human autoimmune insulin dependent diabetes, IDDM. The effector cells of the disease have been shown to be T cells, but also B cells seem to contribute. Adult NOD mice have been shown to display a
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=pmid________::78a5ca0f8e448474b46c94957b8c2e6c
https://pubmed.ncbi.nlm.nih.gov/11696198
https://pubmed.ncbi.nlm.nih.gov/11696198
Publikováno v:
Cytokine. 11(10)
The NOD mouse is an animal model for insulin-dependent diabetes with many similarities to the human disease. NOD mice which are transgenic for the Ea gene, allowing expression of the E molecule, are protected from diabetes and rarely develop insuliti
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::fba725c84373ed341dd0b5cfbbc078cc
https://pubmed.ncbi.nlm.nih.gov/10525315
https://pubmed.ncbi.nlm.nih.gov/10525315
Publikováno v:
Immunology letters. 42(3)
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::653d3dde89b1ad01ae7723a5a79eb438
https://pubmed.ncbi.nlm.nih.gov/7890322
https://pubmed.ncbi.nlm.nih.gov/7890322
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Publikováno v:
Journal of the Medical Association of Thailand; Oct2024, Vol. 107 Issue 10, p778-785, 8p