induction of type 1 diabetes in diabetes-resista nt (bb-dr) rats

نویسندگان

leili yazdchi -marandi from the *immunology department, faculty of medicine, tabriz university of medical sciences, tabriz, iran,and the **departments of immunology and medicine, sunnybrook and women s college health sciences center, university of toronto, toronto, ontario, canada

sheela ramanathan the departments of immunology and medicine, sunnybrook and women s college health sciences center, university of toronto, toronto, ontario, canada

philippe poussier the departments of immunology and medicine, sunnybrook and women s college health sciences center, university of toronto, toronto, ontario, canada

چکیده

the biobreeding- diabetes prone (bb-dp) rat spontaneously develops an autoimmune diabetic syndrome that is dependent on the rt1 u major histocompatibility complex (mhc) haplotype and homozygosity for an allele at the lymphopenia (lyp) locus. lyp mutation is responsible for a peripheral t -lymphopenia. there are other genetic loci contributing to diabetes susceptibility in this strain. bb rats carrying wildtype lyp alleles are not lymphopenic and are resistant to spontaneous diabetes (diabetes r esistant [dr]). our study shows that thymectomy and exposure to one sublethal dose of g-irradiation (tx-r) at 4 weeks of age result in the rapid development of insulitis followed by diabetes in 100% of dr rats. administration of cd45rccd4+ tcrcb+ t cells from unmanipulated syngeneic donors immediately after irradiation prevents the disease. splenic t cells from tx -r induced diabetic animals adoptively transfer type 1 diabetes to t-deficient recipients. wag, wf and lew strains are resistant to tx -r induced insulitis/ diabetes. this novel model of tx -r induced diabetes in bb-dr rats can be used to identify environmental and cellular factors that are responsible for the initiation of antipancreatic autoimmunity.

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INDUCTION OF TYPE 1 DIABETES IN DIABETES-RESISTA NT (BB-DR) RATS

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عنوان ژورنال:
medical journal of islamic republic of iran

جلد ۱۸، شماره ۴، صفحات ۳۶۵-۳۷۰

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