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)

Graft-versus-host disease (GVHD) is an immunologically mediated disease occurring most frequently after allogeneic bone marrow transplantation. The aim of this study was to evaluate the contribution of immunohistochemistry in the diagnosis of cutaneous GVHD. Patients transplanted for either leukemia or beta-thalassemia were included in the study. Skin lesions of acute and chronic GVHD were examined both by direct immunofluorescence to detect immunoglobulin deposits and by an avidin-biotin-peroxidase complex technique to evaluate the inflammatory cell infiltrate. Epidermal and dermal fluorescent bodies (IgG and IgM) were frequently found in both acute and chronic GVHD. Most of the infiltrating cells were CD3+ T lymphocytes, with CD8+ cells representing the major cell population invading the epidermis both in acute GVHD and in chronic lichenoid GVHD. A small proportion of the dermal cells were CD14+ macrophages; no B cells were detected. HLA-DR, but not HLA-DQ antigens, were variably expressed by keratinocytes in all cases of acute GVHD and in chronic lichenoid GVHD. KL-1, a monoclonal antikeratin antibody specific for the 56.5 KD acidic polypeptide usually present in suprabasal keratinocytes, stained all epidermal layers, including the basal layer. Langerhans cells were dramatically reduced in number in the epidermis of both acute and chronic lichenoid GVHD. It is concluded that immunohistologic analysis may be supportive in the diagnosis of acute and early chronic lichenoid cutaneous GVHD.
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PMID:Immunohistochemistry of cutaneous graft-versus-host disease after allogeneic bone marrow transplantation. 193 60

In this study we examined the effects of acute graft-vs-host disease (aGVHD) on the Brown Norway (BN) rat liver. When clinical signs of the disease appeared, rats were inoculated with fluorescent latex beads and 30 min later nonparenchymal cells were isolated from the liver. The cells were then analyzed via flow cytometry, histochemistry, and electron microscopy. Flow cytometry demonstrated that 58% of the cells from the 80 ml/min elutriation fraction (normally rich in Kupffer cells) of the non-GVHD liver had high fluorescence intensity compared to 8% in rats with aGVHD. Determination of the cellular composition of the various fractions with electron microscopy confirmed flow cytometry observations in that only 9% of the 80 ml/min elutriation fraction of GVHD livers had peroxidase-positive rough ER and the morphological appearance of macrophages as compared to 60% in the non-GVHD liver. The low percentage of fluorescent-positive Kupffer cells in the 80 ml/min elutriation fraction of the GVHD liver is attributed to a massive lymphocytic invasion of the liver and not necessarily to a defect in the mononuclear phagocyte system.
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PMID:Effects of acute graft-vs-host disease on the liver of the brown Norway rat. 347 36

Granulocyte transfusions have been complicated by graft-versus-host disease (GVHD) in the recipients. This risk can be eliminated by irradiation of the cell product. The effect of in vitro irradiation on elements of lymphocyte and granulocyte function was therefore studied in order to determine the dose of irradiation which blocked lymphocyte function without affecting the function of granulocytes. Lymphocyte blast transformation after stimulation with mitogens was reduced by 90% after irradiation with 1500 rad and by 97% after 5 000 rad. The response to microbial agents and allogeneic cells was far more radio-sensitive, being completely abolished after irradiation with 1 000 and 500 rad, respectively. Mobility was the function of polymorphonuclear leucocytes (PMN) most affected by irradiation, being slightly but significantly reduced after irradiation with 10 000-20 000 rad. The bactericidal activity was reduced only after irradiation with 40 000 rad or more, while the hexose monophosphate shunt activity and the myeloperoxidase activity were largely unaffected by irradiation with doses of up to 120 000 rad. Hence the results indicate that the irradiation of leucocytes intended for transfusion with a dose of 2 000 rad is likely to prevent GVHD without causing any apparent damage to the PMN.
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PMID:Effect of in vitro X-irradiation on lymphocyte and granulocyte function. 646 Oct 60

Previous studies have revealed quantitative alterations in laminin-1 expression at the mRNA and protein levels during the development of glomerulonephritis and glomerulosclerosis in chronic graft-versus-host disease in mice, a model for lupus nephritis. We have now studied the qualitative alterations in laminin expression with two monoclonal antibodies that recognize epitopes on either the E8 or the P1 fragment of laminin-1. Both of these fragments are involved in cell-matrix and matrix-matrix interactions. In normal glomeruli these laminin epitopes are present only in the mesangial matrix; during embryogenesis, however, they are also present in the glomerular basement membrane. The distribution of laminin epitopes was first studied by using immunofluorescence in kidneys of mice with graft-versus-host disease at different points in time after disease induction. Reflection contrast and immunoelectron microscopy were performed after in vivo injection of the horseradish peroxidase-coupled monoclonal antibodies. In glomeruli of mice 8 weeks after disease induction, both injected antibodies bound specifically in electron-dense immune deposits in the mesangium and subepithelially along the glomerular basement membrane as well as in the expanded mesangial matrix. At 11 and 12 weeks after disease induction, when focal and segmental glomerulosclerosis had developed, the antibodies additionally bound in the matrix subendothelially along the glomerular basement membrane and at the periphery of end-stage sclerotic lesions. To study changes in the distribution of laminin epitopes over time, mice were injected with either monoclonal antibody before induction of graft-versus-host disease. The antibodies were detected 8 and 12 weeks later in the mesangial matrix of mice with lupus nephritis. Once segmental glomerulosclerosis had developed, the antibodies were additionally detected within the thickened glomerular capillary wall. The specific binding of anti-laminin monoclonal antibodies in electron-dense immune deposits further substantiates the hypothesis that anti-laminin autoantibodies participate in glomerular immune complex formation in this model, as suggested by earlier studies. Furthermore, our results show that the distribution of glomerular laminin epitopes in the matrix is altered during the development of glomerular disease. These changes in the structure of the glomerular basement membrane may contribute to the abnormal cell-matrix and matrix-matrix interactions during the development of glomerular disease in this model for lupus nephritis.
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PMID:Qualitative alterations in laminin expression in experimental lupus nephritis. 754 36

A 'sandwich' enzyme-linked immunosorbent assay has been developed for measuring humanized anti-Tac (HAT), a humanized antibody to the IL-2 receptor on activated T cells (Tac), in human serum. The working range of this assay is 25-400 ng/ml with an overall precision of 5%. In this assay, the analyte, HAT, is sandwiched between Tac which is bound to a microtiter plate and biotinylated Tac that is conjugated to peroxidase labelled streptavidin. This assay was utilized to determine the pharmacokinetic parameters of HAT in patients with graft-versus-host disease.
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PMID:Determination of humanized anti-Tac in human serum by a sandwich enzyme linked immunosorbent assay. 756 Nov 47

A technique for the rapid detection of cytomegalovirus (CMV) antigen-positive blood leucocytes (CMV antigenaemia) was evaluated in 15 marrow transplant patients as a means of diagnosis and for monitoring CMV-associated disease. CMV antigenaemia was determined by direct immunoperoxidase staining of leucocytes with a peroxidase-labelled monoclonal antibody, HRP-C7, which binds an immediate-early antigen of human CMV. CMV antigenaemia occurred in 7/15 marrow transplant patients (47%) and was initially detected between 4 and 6 weeks after transplantation. CMV-associated diseases developed in 3/15 patients (20%). All patients with CMV-associated disease had a relatively large number of CMV antigen-positive leucocytes, exceeding 10 per 50,000 white blood cells (WBCs). In the remaining 12 patients, CMV antigen-positive leucocytes were less than 10 per 50,000 WBCs or were undetectable. CMV-associated disease did not develop in these patients during the period of monitoring. CMV antigen-positive leucocytes were detected more frequently in patients who developed acute graft-versus-host disease (GVHD) or haemorrhagic cystitis than in those without such complications. CMV antigens were detectable from 1 to 4 weeks before the onset of CMV-associated disease which allowed initiation of ganciclovir treatment at an early stage. The degree of CMV antigenaemia paralleled the clinical symptoms and signs, higher degrees of antigenaemia being associated with more significant disease. Thus, the detection of CMV antigen-positive blood leucocytes is useful for the diagnosis and monitoring of CMV-associated disease following bone marrow transplantation.
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PMID:Cytomegalovirus (CMV) antigenaemia for rapid diagnosis and monitoring of CMV-associated disease after bone marrow transplantation. 787 98

For the differential diagnosis of pulmonary infiltrates after bone marrow transplantation, cytomegalovirus (CMV) antigenemia was evaluated in 9 episodes of pneumonia which developed in 7 allogeneic marrow transplant patients between 9 and 495 days after transplant. The diagnosis of lung infiltration was made based on clinical findings including histological, cytological or microbiological examinations using bronchoalveolar lavage fluid specimens, sputum or lung tissue. The CMV antigen-positive leukocytes were detected with a direct immunoperoxidase technique using a peroxidase-labeled monoclonal antibody (HRP-C7) against CMV immediate early antigen. The episodes included 2 CMV pneumonias, 1 pneumocystis carinii pneumonia, 1 adenovirus pneumonia, 1 bacterial pneumonia, 1 bacterial and fungal pneumonia, 2 idiopathic pneumonias and 1 capillary leak syndrome associated with hyper acute GVHD. The CMV antigenemia became positive only in two patients with CMV pneumonia and the number of CMV antigen-positive leukocytes exceeded 10 per 50000 WBCs. The CMV antigenemia test required only 24 hours to obtain results. These observations suggest that the detection of CMV antigenemia is of great value in the differential diagnosis of pulmonary infiltrates in marrow transplant patients.
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PMID:[Cytomegalovirus antigenemia in the differential diagnosis of pulmonary infiltrates after allogeneic bone marrow transplantation]. 825 5

Several investigations have demonstrated aberrant expression of HLA-DR on damaged bile duct epithelium of patients with primary biliary cirrhosis, liver allograft rejection, graft versus host disease, and AIDS. Since bile duct damage is a prominent feature of chronic hepatitis C, it may also be associated with HLA-DR induction. Therefore, we examined the expression of HLA-DR antigen in formalin-fixed, paraffin-embedded liver biopsy sections of 30 patients with chronic hepatitis C by the avidin-biotin peroxidase complex method using a monoclonal antibody to HLA-DR. HLA-DR was not detected on bile duct epithelium in any of the cases, although bile duct damage of varying degree was observed in 90% of the cases. HLA-DR was expressed by Kupffer cells; inflammatory infiltrates in portal tracts, and in areas of piecemeal necrosis and lobular necrosis; dendritic cells in portal and periportal areas; and occasionally hepatocytes. These observations suggest that the mechanism of bile duct injury in chronic hepatitis C may be different from that of other conditions such as primary biliary cirrhosis, liver allograft rejection, and graft versus host disease.
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PMID:HLA-DR expression in bile duct damage in hepatitis C. 761 62

Manifestations of autoimmune diseases are common in patients who have received allogeneic bone marrow transplantation (BMT). Autoantibodies have been reported in these patients but the source and clinical significance of these autoantibodies are still obscure. In the present study the kinetics of autoantibody formation and the reconstitution of CD5+ B cells was followed in 21 patients who were submitted to allogeneic BMT. Anti-nuclear, anti-smooth muscle, anti-neutrophil cytoplasmic antibodies, anti-reticulin and rheumatoid factor were found at a frequency of 25%, 17%, 24%, 22% and 10% respectively after BMT. Anti-double stranded DNA levels were mildly elevated in 15% of samples. The screening for anti-extractable nuclear antigen, anti-mitochondrial, anti-gastric parietal cell, anti-proteinase III, anti-myeloperoxidase, anti-lactoferrin antibodies was negative. The percentage and absolute count of CD5+ B cells increased with time after allogeneic BMT. Those patients with anti-nuclear or anti-smooth muscle antibodies had significantly higher CD5+ B cell counts than those without these two antibodies. Correlations of CD5+ B cell counts with other autoantibodies were negative. Acute graft-versus-host disease (GVHD) occurred in eight of the patients and chronic GVHD in four patients, but the frequency of autoantibodies had no relationship with the occurrence of acute or chronic GVHD.
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PMID:Autoantibody formation after allogeneic bone marrow transplantation: correlation with the reconstitution of CD5+ B cells and occurrence of graft-versus-host disease. 921 39

Primary biliary cirrhosis (PBC) and graft-versus-host disease (GVHD) are thought to have common immunopathologic features and previous studies have reported that 5.2 to 81% of patients with chronic GVHD after allogeneic hematopoietic cell transplant have antimitochondrial antibodies (AMA). We studied a total of 89 patients with chronic GVHD and 60 controls for AMA reactivity by ELISA and immunoblotting using recombinant PDC-E2, BCOADC-E2, and OGDC-E2, immunoblotting of beef heart mitochondrial proteins, and reactivity to nuclei, smooth muscle (ASMA), ribonucleoprotein JO-1, extractable nuclear antigen, nuclear proteins SSA/ SSB, ribonucleic P proteinase III, cardiolipin (ACA), liver kidney microsomal, thyroid microsomal, myeloperoxidase, and the reactivity of rheumatoid factor. A subset of 60 chronic GVHD sera were tested for reactivity to gp210 and LBR. Finally, liver tissue from patients with chronic GVHD and PBC was studied by immunohistochemistry to determine whether there was comparable abnormal apical staining of biliary epithelial cells using PDC-E2-specific monoclonal antibodies. Surprisingly, there were no AMA found in the sera from the 89 patients with chronic GVHD. Review of published data on AMA in GVHD suggests that previous results were primarily false positives. In contrast, sera from the patients with GVHD did have a variety of other autoantibodies and, in particular, 20/89 (22.4%) positive ANA, 23/89 (25.8%) positive ASMA, and 9/89 (10.1%) positive ACA. The other autoantibodies assayed were not statistically different from controls. Finally, abnormal biliary epithelial luminal staining of bile ducts was found, as expected, in liver tissue of patients with PBC but was absent in chronic GVHD.
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PMID:Autoantibodies in human chronic graft-versus-host disease after hematopoietic cell transplantation. 1021 61


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