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. 2005 Jun;5(6):1286-96.
doi: 10.1111/j.1600-6143.2005.00880.x.

Progression of alloresponse and tissue-specific immunity during graft coronary artery disease

Masashi Tanaka  1 , Monika Zwierzchoniewska, Golnaz K Mokhtari, Raya D Terry, Leora B Balsam, Robert C Robbins, Eugenia V Fedoseyeva
Affiliations
Free article

Progression of alloresponse and tissue-specific immunity during graft coronary artery disease

Masashi Tanaka et al. Am J Transplant. 2005 Jun.
Free article

Abstract

Chronic rejection remains the major obstacle for long-term transplant survival. Both indirect alloresponse and tissue-specific autoimmunity have been implicated in its pathogenesis. The interrelationship between these two types of host anti-graft response remains poorly understood. We have developed an immunosuppression-free mouse model of graft coronary artery disease (GCAD), in which all FVB (H-2(q)) cardiac allografts placed into minor Ag (mHC)-mismatched DBA/1 (H-2(q)) hosts survived more than 112 days, and developed GCAD. We then examined the kinetics of both anti-mHC alloresponse and host autoimmunity against heart-specific antigen, cardiac myosin (CM). At 8 days post-transplantation, recipient mice showed minimal intragraft inflammation and apoptosis, and limited expansion of allo-specific T cells. In addition, we observed early production of anti-myosin IgG1 autoantibodies, which occurred in the absence of activated CM-specific T lymphocytes. By day 56, GCAD indices, the numbers of mHC- and CM-reactive T cells, and the levels of circulating allo- and CM-specific antibodies were all significantly increased. While host alloresponse was exhausted at 112 days post-transplant, T-cell reactivity against CM persisted. Our data suggest that both allo- and tissue-specific immunity might contribute to the induction of GCAD. They indicate that continual autoimmune response against graft tissue antigens may provide for GCAD sustenance.

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