Resistance to the induction of mixed chimerism in spontaneously diabetic NOD mice depends on the CD40/CD154 pathway and donor MHC disparity
HOW DO WE BEST EMPLOY ANIMAL MODELS FOR TYPE 1 DIABETES AND MULTIPLE SCLEROSIS?, cilt.1103, ss.94-102, 2007 (SCI-Expanded, Scopus)
- Yayın Türü: Makale / Tam Makale
- Cilt numarası: 1103
- Basım Tarihi: 2007
- Doi Numarası: 10.1196/annals.1394.015
- Dergi Adı: HOW DO WE BEST EMPLOY ANIMAL MODELS FOR TYPE 1 DIABETES AND MULTIPLE SCLEROSIS?
- Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus
- Sayfa Sayıları: ss.94-102
- Gazi Üniversitesi Adresli: Evet
Özet
Blockade of CD40/CD154 pathway has proven effective in promoting the induction of allogeneic mixed chimerism. Using NOD mouse model of human type 1 diabetes, we investigated whether allogeneic mixed chimerism can be induced in prediabetic NOD mice and in spontaneously diabetic NOD mice under nonmyeloablative and irradiation-free conditioning therapy and anti-CD154 mAb as a short-term posttransplant treatment. We found that spontaneously diabetic NOD mice under nonmyeloablative and irradiation-free conditioning therapy and anti-CD154 mAb as a short-term posttransplant treatment. We found that spontaneously diabetic NOD mice are more resistant to the induction of allogenic mixed chimerism than prediabetic NOD mice under our nonmyeloblative and irradiation-free conditioning therapy. This alloresistance in spontaneously diabetic NOD mice is dependent on the CD40/CD154 pathway and donor MHC disparity.