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Adhesion molecule expression in human hepatic graft-versus-host disease
J Norton1, N al-Saffar, J P Sloane
1Department of Histopathology, Royal Marsden Hospital, Sutton, Surrey, UK.
Bone Marrow Transplantation
|August 1, 1992
Summary
Cellular adhesion molecule expression differs in the liver during graft-versus-host disease (GVHD). Unlike other tissues, ICAM-1, VCAM-1, and ELAM-1 showed limited upregulation in the liver of bone marrow transplant recipients with GVHD.
Area of Science:
- Immunology
- Transplantation Biology
- Cellular Biology
Background:
- Cellular adhesion molecules (ICAM-1, VCAM-1, ELAM-1) play roles in immune responses.
- Graft-versus-host disease (GVHD) involves immune attacks on host tissues after transplantation.
- Understanding adhesion molecule distribution is crucial for diagnosing and managing GVHD.
Purpose of the Study:
- To investigate the distribution of ICAM-1, VCAM-1, and ELAM-1 in normal liver and in liver biopsies from allogeneic bone marrow transplant (BMT) recipients.
- To compare adhesion molecule expression in hepatic GVHD with expression in other GVHD target organs.
Main Methods:
- Immunohistological analysis of liver biopsies.
- Detection of intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), and endothelial-leukocyte adhesion molecule-1 (ELAM-1).
- Comparison between normal liver controls and BMT recipients with and without hepatic GVHD.
Main Results:
- In normal liver, ICAM-1 was on vascular endothelium and sinusoidal cells; VCAM-1 was on Kupffer cells and macrophages. ELAM-1 was largely absent.
- In BMT recipients with hepatic GVHD, ICAM-1 was minimally expressed on damaged bile duct epithelium.
- Increased VCAM-1 positive macrophages were observed in GVHD and non-GVHD liver pathologies, but vascular endothelial expression of VCAM-1 and ELAM-1 did not increase.
Conclusions:
- Adhesion molecule expression patterns in the liver during GVHD differ significantly from those observed in the skin and gastrointestinal tract.
- The limited upregulation of ICAM-1, VCAM-1, and ELAM-1 in the liver may be influenced by biopsy timing, immunosuppressive therapy, or inherent tissue-specific responses.
- These findings highlight potential variations in the cellular and molecular mechanisms of GVHD across different organs.