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Control of Autoimmune diabetes in NOD mice by GAD expression or Suppression in Beta cells presented By Leslie Wattkis.
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Control of Autoimmune diabetes in NOD mice by GAD expression or Suppression in Beta cellspresented By Leslie Wattkis Yoo, J., C. Yoon, H. Lim, Q. Huang, Y. Kang, K. Pyun, K. Hirasawa, R. Sherwin, and H. Jun. 1999. Control of autoimmune diabetes in NOD mice by GADExpression or suppression in β cells. Science. 284: 1183-1186.
Introduction • Atuoimmune diabetes • Glutamic acid decarboxylase (GAD) • Beta Cell-specific suppression • Nonobese diabetic (NOD) • Antisense GAD • Rat insulin promoter (RIP) • Transgenic mice • T-cells proliferation
Suppression of GAD • Protein imunoBlot analysis • GAD Expression • Transgenetic NOD
Expression of antisense GAD gene at cDNA level The establishment of antisense GAD 65.67 transgenic NOD mice
Suppression of GAD Expression Affects • E and F are Islet cells • G and H are salivary cells
GAD expression in the -cells and development of autoimmune diabetes in NOD mice • H-AS GAD mice developed diabetes by 40 weeks of age. • Negative GAD • Tg(-) comparison
Conclusion • GAD must be present at all times for the beta cells to stimulate antigens. • GAD is significant for the autoimmune onset of diabetes type1
Reference • CONTROL OF AUTOIMMUNE DIABETES IN NOD MICE BY GAD EXPRESSION OR SUPPRESSION IN [small beta, Greek] CELLS; Volume 284(5417) pp11183-1187; 14 May 1999 Yoon, Ji-Won; Yoon, Chang-Soon; Lim,Hye-Won; Huang, Qi Quan; Kand, Yupp; Pyun, Kwang Ho; Hirasawa, Kensuke; Sherwin, Robert S.;Jun, Hee-Sook