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[ subject:"Immunology." ]
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The Roles of Iddm30 and Iddm24 in th...
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Chao, Ying-Chieh Gary.
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The Roles of Iddm30 and Iddm24 in the Immunopathogenesis of Type 1 Diabetes in BioBreeding Rats.
紀錄類型:
書目-電子資源 : Monograph/item
正題名/作者:
The Roles of Iddm30 and Iddm24 in the Immunopathogenesis of Type 1 Diabetes in BioBreeding Rats./
作者:
Chao, Ying-Chieh Gary.
面頁冊數:
190 p.
附註:
Source: Dissertation Abstracts International, Volume: 77-06(E), Section: B.
Contained By:
Dissertation Abstracts International77-06B(E).
標題:
Immunology. -
電子資源:
http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3742710
ISBN:
9781339353050
The Roles of Iddm30 and Iddm24 in the Immunopathogenesis of Type 1 Diabetes in BioBreeding Rats.
Chao, Ying-Chieh Gary.
The Roles of Iddm30 and Iddm24 in the Immunopathogenesis of Type 1 Diabetes in BioBreeding Rats.
- 190 p.
Source: Dissertation Abstracts International, Volume: 77-06(E), Section: B.
Thesis (Ph.D.)--University of Toronto (Canada), 2015.
A successful approach to gain insights into the mechanisms underlying genetic association is to map disease-related sub-phenotypes. We focused on the beta cell-overexpression of Ccl11and the differential proportions of inhibitory splenic macrophages in BB rats. We observed a timedependent pancreatic upregulation of Ccl11, as well as a three-fold proportional splenic macrophage increase in BBDP rats compared to T1D-resistant ACI.1u.lyp animals. Through linkage-analysis of a cross-intercross of these two parental strains, these traits mapped to a chromosome 12 region that overlaps with Iddm30. Linkage analysis was confirmed by the BB.ACI-Iddm30 congenic line, where the BBDP allele is associated with increased pancreatic expression of Ccl11, increased proportion and inhibitory function of splenic macrophages; however, the same allele confers T1D-resistance. Analysis of islet-infiltrating T cells in Iddm30 congenic animals revealed that overexpression of pancreatic Ccl11, a prototypical Th2 chemokine, is associated with an enrichment in Th2 CD4+ T cells within the insulitic lesions. We also observed differential NO release by splenic macrophages from congenic animals that correlated with the ability of these cells to inhibit T cell activation. These results indicated that in BBDP rats, Iddm30 controls T1D-susceptibility through both the regulation of Ccl11 expression in beta cells and the subsequent Th1/Th2 balance within islet-infiltrating T-lymphocytes, and raises the questions as to whether the inhibitory effect of splenic macrophages on T cell activation regulates disease risk.
ISBN: 9781339353050Subjects--Topical Terms:
611031
Immunology.
The Roles of Iddm30 and Iddm24 in the Immunopathogenesis of Type 1 Diabetes in BioBreeding Rats.
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A successful approach to gain insights into the mechanisms underlying genetic association is to map disease-related sub-phenotypes. We focused on the beta cell-overexpression of Ccl11and the differential proportions of inhibitory splenic macrophages in BB rats. We observed a timedependent pancreatic upregulation of Ccl11, as well as a three-fold proportional splenic macrophage increase in BBDP rats compared to T1D-resistant ACI.1u.lyp animals. Through linkage-analysis of a cross-intercross of these two parental strains, these traits mapped to a chromosome 12 region that overlaps with Iddm30. Linkage analysis was confirmed by the BB.ACI-Iddm30 congenic line, where the BBDP allele is associated with increased pancreatic expression of Ccl11, increased proportion and inhibitory function of splenic macrophages; however, the same allele confers T1D-resistance. Analysis of islet-infiltrating T cells in Iddm30 congenic animals revealed that overexpression of pancreatic Ccl11, a prototypical Th2 chemokine, is associated with an enrichment in Th2 CD4+ T cells within the insulitic lesions. We also observed differential NO release by splenic macrophages from congenic animals that correlated with the ability of these cells to inhibit T cell activation. These results indicated that in BBDP rats, Iddm30 controls T1D-susceptibility through both the regulation of Ccl11 expression in beta cells and the subsequent Th1/Th2 balance within islet-infiltrating T-lymphocytes, and raises the questions as to whether the inhibitory effect of splenic macrophages on T cell activation regulates disease risk.
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Ccr5 is a candidate gene for Iddm24.1 and we reported on multiple SNPs within the coding and promoter regions of the BBDP allele. Compared to the wild type WF allele, the BBDP variant of Ccr5 was expressed at greater levels. In addition, coding region polymorphisms result in amino acid substitutions of 2 adjacent residues located within the second extracellular loop, necessary for ligand binding. Assessment of signal strength through calcium flux analysis revealed that these polymorphisms mediated stronger signal transduction in the BBDP variant compared to the WF in response to its ligands, Ccl4 and Ccl5. We observed T cells expressing the BBDP Ccr5 variant to be more diabetogenic than their WF Ccr5 expressing counterparts, due to their increased ability to home to the pancreatic islets. iii.
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http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3742710
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