Mice carrying the GFAP-B2m transgene and homozygous for the B2mtm1Unc allele, commonly referred to as GFAP-B2m, are viable, fertile and diabetes resistant. Western blot analysis and histological analysis of brain and pancreas confirmed transgene expression in the astrocytes and peri-islet Schwann cells. FACs analysis indicates the absence of CD8+ T cells in the spleens of both NOD.GFAP-B2m and NOD.B2m deficient mice. Similar to the NOD.B2m deficient mice, NOD.GFAP-B2m mice do not develop spontaneous diabetes by forty weeks of age. In adoptive transfer experiments NOD.GFAP-B2m mice receiving splenocytes from diabetic NOD females develop diabetes at a significantly faster rate and higher incidence than non-transgenic littermates. No diabetes occurred in NOD.GFAP-B2m mice receiving splenocytes from AI4 TCR transgenic mice.
This strain is useful for studying the role of GFAP in autoimmunity and the development of immunotherapies.

This GFAP-B2m transgenic, B2m deficient strain expresses the GFAP-B2m transgene in astrocytes and peri-islet Schwann cells. This strain is resistant to spontaneous diabetes, yet when MHC class 1 is restored in adoptive transfer studies diabetes is accelerated.  These mice are useful to study the role of neuronal autoantigen GFAP in autoimmunity and immunotherapy development.

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