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Related Experiment Video

Updated: Jun 11, 2026

Mouse Model of Alloimmune-induced Vascular Rejection and Transplant Arteriosclerosis
07:05

Mouse Model of Alloimmune-induced Vascular Rejection and Transplant Arteriosclerosis

Published on: May 17, 2015

Alloimmunity and autoimmunity in chronic rejection.

Anil Seetharam1, Venkataswarup Tiriveedhi, T Mohanakumar

  • 1Division of Gastroenterology, Department of Surgery, Washington University School of Medicine, 660 S. Euclid Avenue, St. Louis, MO 63110, USA.

Current Opinion in Organ Transplantation
|July 9, 2010
PubMed
Summary

Alloimmune responses after organ transplant can trigger autoimmunity, leading to chronic rejection. Identifying antibodies to self-antigens may reveal chronic rejection causes and serve as biomarkers.

Related Experiment Videos

Last Updated: Jun 11, 2026

Mouse Model of Alloimmune-induced Vascular Rejection and Transplant Arteriosclerosis
07:05

Mouse Model of Alloimmune-induced Vascular Rejection and Transplant Arteriosclerosis

Published on: May 17, 2015

Area of Science:

  • Immunology
  • Transplantation Science

Background:

  • Alloimmune responses are increasingly implicated in the loss of self-tolerance post-transplant.
  • This can lead to autoimmune responses against self-antigens, contributing to chronic rejection.

Purpose of the Study:

  • To review recent findings on how alloimmune responses induce de novo autoimmune responses after solid organ transplantation.
  • To discuss the implications of these findings for understanding chronic rejection.

Main Methods:

  • Review of recent studies on alloimmunity and autoimmunity in transplantation.
  • In vivo murine model studies demonstrating anti-MHC class I effects on chronic rejection.
  • In vitro studies on epithelial cell responses to anti-MHC ligation.

Main Results:

  • Development of anti-human leukocyte antigen antibodies precedes chronic rejection.
  • Administration of anti-major histocompatibility complex (MHC) class I induces chronic rejection pathology in a murine model.
  • Ligation of MHC class I on epithelial cells can promote cell activation and fibrinogenic growth factor production.

Conclusions:

  • Alloimmune responses can induce autoimmunity, playing a key role in chronic rejection pathogenesis.
  • Characterizing self-antigen antibodies can provide insights into chronic rejection.
  • These antibodies may serve as valuable clinical biomarkers for chronic rejection.