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Updated: May 27, 2026

Induction of Alloantigen-specific Anergy in Human Peripheral Blood Mononuclear Cells by Alloantigen Stimulation with Co-stimulatory Signal Blockade
11:55

Induction of Alloantigen-specific Anergy in Human Peripheral Blood Mononuclear Cells by Alloantigen Stimulation with Co-stimulatory Signal Blockade

Published on: March 14, 2011

Chronic alloantibody mediated rejection.

R Neal Smith1, Robert B Colvin

  • 1Department of Pathology, Massachusetts General Hospital and Harvard Medical School, Boston, MA 02114, USA. rnsmith@partners.org

Seminars in Immunology
|November 5, 2011
PubMed
Summary
This summary is machine-generated.

Alloantibodies are key drivers of acute and chronic antibody-mediated rejection (CAMR). Understanding CAMR

Related Experiment Videos

Last Updated: May 27, 2026

Induction of Alloantigen-specific Anergy in Human Peripheral Blood Mononuclear Cells by Alloantigen Stimulation with Co-stimulatory Signal Blockade
11:55

Induction of Alloantigen-specific Anergy in Human Peripheral Blood Mononuclear Cells by Alloantigen Stimulation with Co-stimulatory Signal Blockade

Published on: March 14, 2011

Area of Science:

  • Transplantation immunology
  • Nephrology
  • Pathology

Background:

  • Alloantibodies are implicated in acute antibody-mediated rejection.
  • Evidence suggests alloantibodies also play a pathogenic role in chronic antibody-mediated rejection (CAMR).
  • CAMR pathogenesis is complex due to slow disease evolution, immunosuppression, and variable alloantibody titers and targets.

Purpose of the Study:

  • To review pathological factors in CAMR diagnosis.
  • To discuss the time course and natural history of CAMR.
  • To explore CAMR pathogenesis, including alloantibodies, complement, gene activation, and Fc effector function.

Main Methods:

  • Literature review focusing on pathological factors, pathogenesis, and therapy of CAMR.
  • Discussion of current and potential therapeutic strategies and their limitations.

Main Results:

  • Alloantibodies are central to both acute and chronic antibody-mediated rejection.
  • CAMR pathogenesis involves complex interactions including complement activation and Fc effector cell function.
  • Therapeutic options for CAMR are currently limited and problematic.

Conclusions:

  • Alloantibodies are definitively linked to acute antibody-mediated rejection and strongly implicated in CAMR.
  • Further research is needed to elucidate dynamic factors influencing CAMR progression.
  • Effective therapies for CAMR remain a significant clinical challenge.