Yoon J, Chang-Soon Yoon,Hye-Won Lim, Qi Huang, Yup Kang, Kwang, Kensuke Hirasawa, Robert Sherwin, and Hee-Sook Jun. 1999. Control of Autoimmune diabetes in NOD mice by GAD expression or suppression in B cells. Science. 284(14): 1183.1187

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• Yoon J, Chang-Soon Yoon,Hye-Won Lim, Qi Huang,
  Yup Kang, Kwang, Kensuke Hirasawa, Robert
  Sherwin, and Hee-Sook Jun. 1999. Control of
  Autoimmune diabetes in NOD mice by GAD expression
  or suppression in B cells. Science. 284(14)
  1183.1187
• Interpreted by Jaime Elvin

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Diabetes

• Type I Diabetes
• insulin dependent
• progression of T-cell mediated autoimmune
  destruction of pancreatic B cells
• Several B cell autoantigens have been implicated
  in the triggering of GAD

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What is GAD?

• Glutamic acid decarboxylase
• hypothesis of this study was to determine whether
  or not GAD expression is required for the
  development of autoimmune diabetes in NOD mice.
• NOD (nonobese diabetic mice)

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GAD Suppression

• Transgenic mice
• two isoforms
• RIP (Rat insulin promoter)
• Prevention of diabetes in antisense GAD
  transgenic NOD mice is not due to the nonspecific
  effect of an antisense transgenic incorporated
  into chromosomal DNA

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Structure of RIP antisense
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Effect of B cell Specific Suppression
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Figure 3 explanation

• Figure 3B
• Independent variable GAD that is stimulated by
  the splenocytes
• Dependent variable is the cell proliferation,
  which will tell you how much the cells have
  replicated

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Protection from reoccurrence of Diabetes

• Insuilits graded
• find the right measures of insulin
• not due to the nonspecific effect of an antisense
  transgenic incorporated into chromosomal DNA

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Progression of GAD suppressed B cells
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Conclusion

• Results
• GAD implications
• Why it is so important to control diabetes
• The data shows that B cell specific suppression
  of GAD expression is sufficient to nearly
  completely prevent autoimmune diabetes in NOD
  mice
• Future research