Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018133 (graft-versus-host disease)
18,032 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The distribution of three cellular adhesion molecules, ICAM-1, ELAM-1 and VCAM-1, was studied in normal rectal mucosa and in graft-versus-host disease (GvHD) using immunohistological and morphometric techniques. In normal controls, ICAM-1 was demonstrable on endothelial cells and leucocytes within the lamina propria, ELAM-1 on endothelial cells only and VCAM-1 on lamina propria leucocytes, many of which exhibited long dendritic processes surrounding the glands. In GvHD, the enterocytes became positive for ICAM-1 and this was often associated with the presence of intra-epithelial LFA-1+ lymphocytes and macrophages, the latter containing debris of apoptotic cells. The staining was, however, restricted to the luminal membrane of the epithelial cells, raising doubts about the role of ICAM-1 as a ligand for LFA-1 on mucosal leucocytes in rectal GvHD. ELAM-1 expression was increased in GvHD both in terms of the length of positive endothelium and staining intensity. VACM-1 was increased on endothelial cells but not leucocytes in the lamina propria in contrast to our previous findings in cutaneous GvHD where VCAM-1+ dendritic cells were increased and endothelial cells remained negative. Normal patterns of adhesion molecule staining were seen in two biopsies exhibiting no morphological evidence of GvHD, from patients who had strong clinical evidence of the disease, indicating that immunostaining for these molecules is unlikely to be of help in improving the sensitivity of histological diagnosis. However, the possibility that adhesion molecule staining may be useful in improving diagnostic specificity by helping to distinguish GvHD from identical histological changes produced by irradiation and cytotoxic drugs is worthy of further investigation.
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PMID:Expression of adhesion molecules in human intestinal graft-versus-host disease. 137 Sep 27

An immunohistological study of the distribution of three cellular adhesion molecules, ICAM-1, VCAM-1 and ELAM-1, was undertaken on normal liver and liver biopsies taken from allogeneic bone marrow transplant (BMT) recipients. In normal controls, ICAM-1 was seen on vascular endothelium and sinusoidal lining cells, and VCAM-1 on Kuppfer cells and dendritic macrophages in portal tracts. ELAM-1 staining was virtually absent. Biopsies from BMT recipients with histological evidence of hepatic graft-versus-host disease (GVHD) showed ICAM-1 expression on damaged bile duct epithelium in only one of five cases, in contrast to four of five showing epithelial HLA-DR expression. Increased numbers of VCAM-1 positive portal tract macrophages were seen in GVHD and also in non-GVHD pathology. No increase in vascular endothelial expression of VCAM-1 or ELAM-1 was seen. These findings contrast with previous studies on other target sites for GVHD, namely skin and gastrointestinal tract, where the expression of all three molecules is increased on various cells. Although the lack of adhesion molecule expression in the liver in GVHD in this study may be related to the timing of biopsies or immunosuppressive therapy, it is likely to represent to some extent variation in cell and molecular changes occurring in the different tissues affected by GVHD.
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PMID:Adhesion molecule expression in human hepatic graft-versus-host disease. 138 79

Acute graft-versus-host disease is a common complication of allogeneic bone marrow transplantation, but the mechanisms resulting in tissue injury are uncertain. In order to probe the effector phase of upper gastrointestinal acute GVHD, we performed immunopathologic studies of duodenal biopsies obtained from patients with or without GVHD. We evaluated the infiltrating mononuclear cells in both epithelium and lamina propria for expression of CD2, CD4, CD8, CD25, T alpha/beta and gamma/delta receptors, CD16, CD56, CD57 and also studied the distribution of cell adhesion molecules (ELAM-1, VCAM-1, ICAM-1, PECAM-1). In the epithelium, only a minimal T cell infiltrate was observed. In the lamina propria, GVHD tissue (vs. control) had an infiltrate of CD2+ (17.7 +/- 2.9% vs. 7.2 +/- 1.8%; P < 0.04), CD8+ (15.5 +/- 4.4% vs. 4.8 +/- 1.9%, P < 0.04) T lymphocytes. GVHD-positive and control tissues contained similar numbers of CD4+ T cells and natural killer cells (CD56+ or CD57+). ICAM-1 staining of endothelial cells was prominent in GVHD tissues (13.5 +/- 1.1 capillaries/field) and was significantly increased over non-GVHD specimens (7.5 +/- 1.8; P < 0.02). ELAM-1, VCAM-1, and PECAM-1 were similarly distributed in both biopsy groups. These data suggest that effectors of upper GI GVHD include CD2+, CD8+, T lymphocytes infiltrating the lamina propria. Inflammatory cell activation and resultant secretion of cytokines might directly damage the mucosa, but may also upregulate ICAM-1 on local endothelium leading to perpetuation of inflammation by recruitment of additional cytotoxic lymphocytes.
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PMID:The immunopathology of upper gastrointestinal acute graft-versus-host disease. Lymphoid cells and endothelial adhesion molecules. 768 Dec 25

The inflammation-associated molecules intercellular adhesion molecule (ICAM)-1, endothelial lymphocyte adhesion molecule (ELAM)-1, vascular cell adhesion molecule (VCAM)-1, human leukocyte antigen (HLA)-DR, interleukin (IL)-2R (CD25), CD34, alpha-1-antichymotrypsin (alpha 1-ACT), and L1 antigen were studied in skin from marrow recipients to determine the timing and distribution of their expression in relation to the clinical and histologic evolution of graft-versus-host disease (GvHD). Four phases were recognized: 1. pretransplant with no immunohistologic change; 2. posttransplant with no evidence of GvHD when dermal alpha 1-ACT + macrophages were increased; 3. posttransplant with clinical, but not histologic, evidence of GvHD with increased keratinocyte HLA-DR and ICAM-1 expression and increased numbers of VCAM-1+ dermal cells; and 4. posttransplant with clinical and histologic evidence of GvHD characterized by an infiltrate of CD25+ T cells, L1+, alpha 1-ACT+ and VCAM-1+ macrophages, L1 antigen expression on keratinocytes accompanied by further increases in HLA-DR and ICAM-1, and increased endothelial ELAM-1 staining with a reciprocal decrease in CD34. A sequential accumulation of cellular and molecular changes, therefore, occurs in the evolution of acute GvHD, and immunostaining for HLA-DR, ICAM-1, and VCAM-1 may be helpful in diagnosing early disease.
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PMID:A prospective study of cellular and immunologic changes in skin of allogeneic bone marrow recipients. Relationship to clinical and histologic features of acute graft-versus-host disease. 817 66

A 20-year-old woman with aplastic anemia underwent bone marrow transplantation from an HLA-identical sibling after total lymphoid irradiation (TLI) and cyclophosphamide (CY). The post-transplant course was uneventful. CYA was discontinued on day 221. Three weeks later, the patient developed cutaneous GVHD precisely localized to the field of TLI. No other organs were involved. Immunohistochemical staining of the affected skin was strongly positive for ICAM-1, PECAM-1 and ELAM-1; normal skin was only weakly positive for ICAM-1. CYA was restarted, and the skin lesions disappeared. TLI may contribute to an unusual presentation of cutaneous GVHD associated with specific expression of adhesion molecules.
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PMID:Cutaneous chronic graft-versus-host disease localized to the field of total lymphoid irradiation. 867 42