Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
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.
 ...
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.
 ...
PMID:Effects of acute graft-vs-host disease on the liver of the brown Norway rat. 347 36

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.
 ...
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.
 ...
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.
 ...
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.
 ...
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.
 ...
PMID:HLA-DR expression in bile duct damage in hepatitis C. 761 62

A 2-year-old Japanese boy who presented with multiple cervical, axillary, and inguinal lymphadenopathy was diagnosed by immunocytochemical analysis as having myeloid/natural killer (NK) cell precursor acute leukemia. Leukemic blasts in the bone marrow were positive for CD56 (NK marker), CD7 (T-cell marker), CD33 (myeloid marker), CD34, and HLA-DR. Tumor cells in a lymph node were also positive for CD2, cytoplasmic CD3 (T-cell marker), CD7, CD33, CD34, and CD56, but negative for peroxidase staining and other T-cell, NK, and myeloid markers. Southern blot analysis showed no rearrangement bands for T-cell receptor delta and immunoglobulin heavy chain. Chromosomal analysis revealed 46,XY,inv(7)(p21q21). Neither chemotherapy for acute lymphoblastic leukemia nor that for acute myeloid leukemia induced remission in this patient. However, complete remission was achieved by the administration of L-asparaginase (6,000 U/m2 for 5 days). Because the disease was considered refractory to standard chemotherapy, cord blood transplantation was performed from an HLA 1-locus mis-matched unrelated donor. The conditioning regimen consisted of total body irradiation, cytarabine, and cyclophosphamide, and cyclosporine and short-term methotrexate were employed for graft-versus-host disease (GVHD) prophylaxis. Hematological reconstitution was rapid, and only grade I acute GVHD was observed. The patient has been in remission for more than 24 months after transplantation. Our findings indicate that combination therapy with L-asparaginase and allogeneic stem cell transplantation may be useful for the treatment of myeloid/NK cell precursor acute leukemia.
 ...
PMID:Treatment of a child with myeloid/NK cell precursor acute leukemia with L-asparaginase and unrelated cord blood transplantation. 1193 70

This article describes a rare case of bone marrow transplantation (BMT) from an unrelated donor (URD) in an adult Japanese male with Down syndrome (DS) diagnosed as having acute mixed lineage leukemia. Examination of peripheral blood demonstrated WBC 6.2 x 10(9)/l with 45.5% blasts at admission. Leukemic blasts with positive peroxidase stain, but negative periodic acid-Schiff stain comprised 91.6% on bone marrow specimen. Surface marker analysis of these blasts showed the following: CD3(-), CD5(-), CD7(-), CD10(+), CD19(+), CD13(+), CD14(-), CD33(+), CD34(+), CD41a(-), and CD56(-). Based on these data, he was diagnosed as having acute mixed lineage (myeloid and B-lymphoid lineage) leukemia. He achieved complete remission (CR) by lymphoid-oriented chemotherapy performed after ineffective myeloid-oriented therapy. After four courses of consolidation chemotherapy for lymphoid lineage blasts, recurrence due to proliferation of myeloblasts had occurred. Thereafter, a second CR was obtained by low dose cytosine arabinoside (AraC) therapy. As this patient was considered to have a high risk of relapse, we selected allogeneic BMT from URD. Severe stomatitis due to methotrexate (MTX) occurred probably due to altered pharmacokinetics usually observed in DS patients. Though acute graft-versus-host disease (GVHD) of systemic skin (grade II) and pneumonia were observed during neutropenia due to the post-conditioning regimen, he could be discharged from our hospital on the 135th day after BMT. On day 205 post-BMT, however, bronchiolitis obliterans (BO) occurred as a chronic GVHD disorder. Despite therapy with prednisolone and FK506, he died on day 400 post-BMT because of respiratory failure due to BO. In DS patients, superfluous toxicities due to MTX and AraC treatment have been reported, and these toxicities have been considered due to altered pharmacokinetics in patients with DS. This patient could tolerate the transplant conditioning regimen commonly used in patients without DS.
 ...
PMID:Unrelated donor bone marrow transplantation for acute mixed lineage (myeloid and B-lymphoid lineage) leukemia in an adult with Down syndrome. 1270 27

This paper describes our own findings on the role of Langerhans' cells in dermatology and discusses literature data on their detection in seven different dermatoses. The skin is an integral part of immune system. During the past 30 years, increasing evidence has been accumulated that the skin contains cellular elements which are needed for the initiation and expression of immune response. Langerhans' cells (LCs) are dendritic cells originating in the bone marrow. They reside mainly within stratified squamous epithelia and constitute approximately 2-4% of epithelial cells. LCs are epidermal antigen presenting cells which play a crucial role in allergic contact hypersensitivity, viral diseases, graft versus host disease and elimination of neo-plastic cell clones. They express antigens conjugated with major histocompatibility complex (MHC) class II positive molecules on their surfaces for presentation to T-helper lymphocytes. LCs cannot be identified in routinely prepared histologic testing but can be visualised at the light microscope level by histochemical and immunologic techniques. Appropriate methods for the detection of Langerhans' cells in dermatology (also shown by our own experience) are histoenzymatic methods of adenosintriphosphatase (ATP-ase), acid phosphatase (AP), alpha-naphthylacetatesterase (ANAE and peroxidase-antiperoxidase immunohistochemistry method with polyclonal S-100 protein antibody (PAP). LCs are the only cells in normal skin with ATP-ase activity. Histoenzymatic methods used in patients with atopic dermatitis, vitiligo, mycosis fungoides, Behcet's disease, lichen ruber planus, psoriasis vulgaris, irritant dermatitis and allergic contact dermatitis demonstrated LSs in epidermis and dermis. ANAE and AP showed concordance and were suitable histochemical markers for LC distribution and macrophages in the dermis in mycosis fungoides, atopic dermatitis, psoriasis vulgaris, irritant chronic dermatitis and Bechet's disease. Our experience of the human skin showed a strong activity of calcium-activated adenosine triphosphatase in LCs. LCs in the guinea pig skin can be demonstrated by Mg++ and Ca++ activated adenosine triphosphatase, but a stronger activity of Ca++ activated adenosine triphosphatase in LCs after irritation. Ca++ ATP-ase as an indicator of energy-dependent pump is the reflection of intracellular calcium level, which is a significant factor for regulating the growth and metabolism of the cells. LCs are found as target cells during the efferent phase of contact allergic reaction. Immunohistochemical methods, define the role of LCs in dermatology more precisely and allow complete immunologic recognition within the epidermis.
 ...
PMID:[Identification of Langerhans cells in dermatology]. 1528 65


1 2 Next >>