Resistance to the induction of mixed chimerism in spontaneously diabetic NOD mice depends on the CD40/CD154 pathway and donor MHC disparity

Bin Luo, Tao Wu, Yisheng Pan, Hakan Sozen, Jianqiang Hao, Yu Zhang, David E.R. Sutherland, Bernhard J. Hering, Zhiguang Guo

Research output: Chapter in Book/Report/Conference proceedingChapter

2 Scopus citations

Abstract

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 shortterm posttransplant treatment. We found that spontaneously diabetic NOD mice are more resistant to the induction of allogeneic mixed chimerism than prediabetic NOD mice under our nonmyeloablative and irradiation-free conditioning therapy. This alloresistance in spontaneously diabetic NOD mice is dependent on the CD40/CD154 pathway and donor MHC disparity.

Original languageEnglish (US)
Title of host publicationHow Do We Best Employ Animal Models for Type 1 Diabetesand Multiple Sclerosis
PublisherBlackwell Publishing Inc
Pages94-102
Number of pages9
ISBN (Print)1573316784, 9781573316781
DOIs
StatePublished - Apr 2007

Publication series

NameAnnals of the New York Academy of Sciences
Volume1103
ISSN (Print)0077-8923
ISSN (Electronic)1749-6632

Keywords

  • Bone marrow transplantation
  • CD154
  • Mixed chimerism
  • NOD mice
  • Type 1 diabetes

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    Luo, B., Wu, T., Pan, Y., Sozen, H., Hao, J., Zhang, Y., Sutherland, D. E. R., Hering, B. J., & Guo, Z. (2007). Resistance to the induction of mixed chimerism in spontaneously diabetic NOD mice depends on the CD40/CD154 pathway and donor MHC disparity. In How Do We Best Employ Animal Models for Type 1 Diabetesand Multiple Sclerosis (pp. 94-102). (Annals of the New York Academy of Sciences; Vol. 1103). Blackwell Publishing Inc. https://doi.org/10.1196/annals.1394.015