Literature DB >> 12100900

Use of recombinase activation gene-2 deficient mice to ascertain the role of cellular and humoral immune responses in the development of chronic rejection.

Hong Sun1, Jennifer E Woodward, Vladimir M Subbotin, Ruhul Kuddus, Alison J Logar, Adam T Schaefer, Abdelouahab Aitouche, Abdul S Rao.   

Abstract

INTRODUCTION: Given its multifactorial etiology, the relative contribution of anti-donor cellular and humoral immune responses in the pathogenesis of chronic rejection is as yet ambiguous. We hypothesized that alloreactive T and B cells play a seminal role in the development of this lesion.
METHODS: To address this hypothesis, RAG-2(-/-) mice were used as donors and recipients in a well-established murine model of aortic transplantation. Grafts were transplanted across the following groups: Group I: C3H --> C3H; Group II: Wild-type [WT] 129Sv (H-2(b)) --> C3H (H-2(k)); Group III: C3H --> WT 129Sv; Group IV: 129SvEv RAG-2(-/-) --> C3H; and Group V: C3H --> 129SvEv RAG-2(-/-). Grafts were harvested at d40 to 146 post-transplantation for morphologic and immunohistochemical analyses and semi-quantitative RT-PCR was employed to evaluate the intragraft mRNA expression of various immune mediators. Mixed lymphocyte reaction and complement-mediated alloantibody cytotoxicity assays were performed to determine anti-donor proliferative and humoral responses, respectively.
RESULTS: Unlike that across the syngeneic combination (Group I), marked intimal thickening with corresponding luminal narrowing was observed in the majority of the aortic allografts (Groups II-IV). On the contrary, the morphology of C3H aortic allografts harvested from the majority of the RAG-2(-/-) was remarkably preserved. Correspondingly, anti-donor proliferative and humoral immune responses were undetectable in C3H --> RAG-2(-/-) recipients as was the intragraft mRNA expression of the Th(1) and the Th(2)-type cytokines.
CONCLUSIONS: Taken together, these data suggest that in this murine model of aortic allotransplantation, donor-specific cellular and humoral responses play a dominant role in the initiation and perpetuation of chronic rejection.

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Year:  2002        PMID: 12100900     DOI: 10.1016/s1053-2498(02)00393-5

Source DB:  PubMed          Journal:  J Heart Lung Transplant        ISSN: 1053-2498            Impact factor:   10.247


  1 in total

1.  Genetic or pharmaceutical blockade of phosphoinositide 3-kinase p110δ prevents chronic rejection of heart allografts.

Authors:  Huijun Ying; Hongmei Fu; Marlene L Rose; Ann M McCormack; Padmini Sarathchandra; Klaus Okkenhaug; Federica M Marelli-Berg
Journal:  PLoS One       Date:  2012-03-30       Impact factor: 3.240

  1 in total

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