ISSN:0022-3417    

DOI:10.1002/path.1711700202

出版商:John Wiley&Sons, Ltd.    

年代:1993

数据来源: WILEY

摘要:

AbstractHepatic fibrosis, a consequence of most forms of chronic liver disease, is a dynamic process involving complex interactions between several cell types, the net result of which is accumulation of several distinct extracellular matrix (ECM) proteins. The resultant disruption of intrahepatic blood flow contributes to the development of portal hypertension. The effects, however, are not merely a space‐occupying phenomenon; by changing the composition of the ECM, fibrosis may also alter hepatocyte function via cellular integrins. The principal source of ECM proteins in normal and fibrotic liver is the perisinusoidal cells which lie in the space of Disse. The response of this cell population to acute and chronic liver injury has been studied in detail. Perisinusoidal cells proliferate and become activated following hepatocyte necrosis. This phenomenon is transient in acute injuries, but in chronic liver disease, continued activation is associated with phenotypic modulation of perisinusoidal cells to myofibroblasts. This process is mediated by various cytokines including TGF‐β and PDGF. Some of the growth factors involved are derived from activated Kupffer cells and there is evidence of a complex interplay between mediators; injured sinusoidal endothelial cells and platelets are possible additional sources. Accumulation of ECM proteins in fibrosis can be explained not only by increased synthesis, but also by decreased degradation. There is growing evidence that in fibrotic liver there is decreased interstitial collagenase activity. This is, at least in part, due to expression of a tissue inhibitor of metalloproteinase, TIMP‐1, by activated perisinusoidal

ISSN:0022-3417    

DOI:10.1002/path.1711700203

出版商:John Wiley&Sons, Ltd.    

年代:1993

数据来源: WILEY

摘要:

AbstractThe development of B‐cell memory is linked to the presence of germinal centres. This process is dependent on the presence of antigen, usually in the form of immune complexes with antibody, on the surface of the follicular dendritic cells (FDCs) that form a network in the germinal centre. The presence of immune complexes poses a constant danger of activating complement. Decay accelerating factor (DAF, CD55) and the membrane attack complex (MAC) inhibitor (CD59) are two cell proteins whose sole function is to protect cells from the action of complement, the former affecting the earlier components of the complement cascade, and the latter the terminal ones; both are bound to the cell surface via a glycosylphosphatidylinositol link. DAF but not CD59 could be demonstrated on FDCs. DAF is also present on the FDCs in follicular lymphomas despite the absence of complement (C3) in neoplastic follicles. This indicates that DAF is constitutive to FDCs but does not preclude the possibility that its expression is increased when immune complexes are deposite

ISSN:0022-3417    

DOI:10.1002/path.1711700204

出版商:John Wiley&Sons, Ltd.    

年代:1993

数据来源: WILEY

摘要:

AbstractIn order to define compartment‐related structures within the extracellular matrix of human lymphoid organs, monoclonal antibodies (MAbs) were generated by immunizing mice with stromal fragments of human tonsils. One MAb (4C7) was selected which recognized an endothelial basal membrane component that is selectively expressed in capillaries of lymphoid follicles. The epitope was also present in follicles within chronically inflamed synovial membrane and in a hyperplastic thymus of a patient with myasthenia gravis. B‐cell non‐Hodgkin's lymphomas with a follicular growth pattern expressed the antigen in neoplastic follicles, whereas diffuse growing lymphomas lacked the antigen. The restricted distribution pattern suggests involvement of the 4C7‐defined antigen in the organization of the follicular compartment within human lymphoid

ISSN:0022-3417    

DOI:10.1002/path.1711700205

出版商:John Wiley&Sons, Ltd.    

年代:1993

数据来源: WILEY

摘要:

AbstractForty‐four cases of Hodgkin's disease (HD), mostly of the nodular sclerosing type, were investigated for the presence of Epstein‐Barr virus (EBV) by polymerase chain reaction (PCR) and DNA and RNAin situhybridization (DISH, RISH), as well as by immunohistochemistry for the detection of latent membrane protein‐1 (LMP‐1) of EBV.in situhybridization (ISH) was combined with immunohistochemistry to correlate the presence and activity of the virus at the cellular level. In 18/34 (53 per cent) cases, EBV‐DNA sequences could be detected with the PCR method. In 12/18 positive cases, DISH and RISH were also positive. In the remaining six EBV‐PCR positive cases, two were also positive with RISH and LMP‐1, whereas no positive signal with DISH could be obtained. All DISH and/or RISH positive cases were also positive for LMP‐1. With RISH, not only the Reed‐Sternberg cells and their mononuclear variants (RS cells) stained positive, but also small and intermediate cells frequently reacted with the EBV‐specific probes (EBER‐1 and ‐2). Double staining with cellular markers (CD3, CD20, CD45, CD45RO, CD68, and the lectin PNA) revealed that most of the smaller EBER‐positive cells frequently did not express T, B, or histiocytic markers, but that they, as well as the RS cells, showed cytoplasmic and membranous staining with PNA. These smaller EBER‐positive cells were not found in EBV‐PCR negative HD. EBER‐positive RS cells were almost always LMP‐1 positive, as well as a substantial proportion of the intermediate‐sized cells, whereas the majority of the small EBER‐positive cells remained LMP‐1 negative. In EBV‐PCR positive non‐malignant lymph nodes, only a few EBER‐1 and ‐2 positive cells could be observed. As in infectious mononucleosis, these cells frequently expressed the B‐cell marker CD20. Although we cannot exclude the fact that the majority of the smaller EBV‐positive cells in HD belong to reactive EBV‐infected lymphocytes, our data favour the hypothesis that at least some of these smaller cells

ISSN:0022-3417    

DOI:10.1002/path.1711700206

出版商:John Wiley&Sons, Ltd.    

年代:1993

数据来源: WILEY

摘要:

AbstractUsing Southern hybridization analysis, we have detected the Epstein‐Barr virus (EBV) genome in 36 per cent (4/11) of enteropathy‐associated T‐cell lymphoma (EATL), a frequency much higher than that seen in nodal T‐cell lymphomas in which we were able to show EBV DNA in only 3 per cent (1/30) of the cases examined. Using a terminal fragment probe, monoclonal proliferation of EBV in infected cells was demonstrated in three of the four EBV‐positive EATL cases (in one case, insufficient signal prevented the determination of EBV clonality). The EBV genome and an early transcript, EBER1, were identified in tumour cells byin situhybridization. Expression of latent membrane protein (LMP) was detected in two EBV DNA/RNA‐positive EATL cases. In view of the known oncogenic properties of EBV and the putative central role of LMP in EBV‐induced cell immortalization, the results of this study suggest that the virus may play an aetiological role in the pathoge

ISSN:0022-3417    

DOI:10.1002/path.1711700207

出版商:John Wiley&Sons, Ltd.    

年代:1993

数据来源: WILEY

摘要:

AbstractEpstein‐Barr virus (EBV) recently has been implicated in the pathogenesis of Hodgkin's disease (HD). Lymphomatoid papulosis (LyP) is a premalignant cutaneous lymphoproliferative disorder which shares several characteristics with HD. The hypothesis has been made that EBV may be associated with the pathogenesis of LyP. We therefore examined 17 skin biopsy specimens and two lymph nodes from nine patients with LyP for EBV RNA using the highly sensitive and specific EBER method. In all specimens, the large atypical cells were negative for EBV while poly T studies confirmed the presence of adequate RNA for detection of EBER. The negative EBER results were confirmed in seven LyP patients whose biopsies were also stained for latent membrane protein (LMP‐1). Interestingly, one patient with clonally related LyP and HD had no EBV RNA detected in any specimen. We conclude that EBV is unlikely to be an important aetiological agent in LyP. If confirmed in other patients, HD associated with LyP may have a different aetiology from HD arisingde n

ISSN:0022-3417    

DOI:10.1002/path.1711700208

出版商:John Wiley&Sons, Ltd.    

年代:1993

数据来源: WILEY

摘要:

AbstractIn a study of 49 biopsies from the margins of depigmented cutaneous lesions in 18 patients with vitiligo, highly significant overall increases were found in CD3+, CD4+, and CD8+ T cells, though cell numbers in individual cases were often within the normal range. Many of the T cells were activated (MHC class II+, interferon gamma+), of CD45RO (UCHL1+) memory subset, and many expressed the cutaneous lymphocyte‐associated antigen (HECA‐452+) typical of skin‐homing T cells. Immunohistologically, the most intense epidermal T‐cell infiltration was present within 0.6 mm of the edge of the lesion in 10 of 13 double‐stained sections with a clearly defined zone of melanocyte depletion. In 40 lesions from 17 patients seen 11–64 weeks after biopsy, no apparent association was found between T‐cell numbers and disease activity as assessed by Köbnerization of biopsy wounds or spread of depigmentation. These findings are consistent with the hypothesis that lesional T cells rather than circulating antimelanocytic antibody may be responsible for the supposedly autoimmune but characteristically patchy destruction of cutaneous melanocytes in vitiligo. Nevertheless, many of the infiltrating T cells are probably innocent bystanders attracted by upregulated cell adhesion molecules near sites of mel

ISSN:0022-3417    

DOI:10.1002/path.1711700209

出版商:John Wiley&Sons, Ltd.    

年代:1993

数据来源: WILEY

摘要:

AbstractExtravasation of leucocytes in tissues is mediated by leucocyte—endothelial cell interactions in which adhesion molecules play an important role. Until now, two pathways have been unravelled, i.e., the LFA‐1/ICAM‐1 and the VLA‐4/VCAM‐1 pathways. ELAM‐1 has been shown to be involved in granulocyte accumulation and recently also in lymphocyte migration. The role of HECA‐452 is under investigation. In this study we have investigated the expression of the above‐mentioned adhesion molecules in lung tissue of patients with pulmonary sarcoidosis and usual interstitial pneumonitis (UIP), and in mediastinal lymph nodes of patients with sarcoidosis. ICAM‐1 (CD54) was broadly distributed on the endothelium of all the vessels found in sarcoidosis and UIP. VCAM‐1 was present on the endothelium of the venules, capillaries, and arterioles in both sarcoidosis and UIP. ELAM‐1 reacted with endothelial cells lining venules and capillaries in chronic progressive sarcoidosis and in the active phase of UIP but not in the stationary phases of both diseases. HECA‐452 activity could be detected only on high endothelial venules within sarcoid lymph nodes. In lung tissues, macrophages bearing the ICAM‐1 antigen were present in sarcoid tissue but not in the interstitium and alveolar space of UIP. LFA‐1 (CD11a/CD18) and VLA‐4 (CD49d/CD29) were present on all leucocytes found but seemed to be more highly expressed on lymphocytes in sarcoidosis. These findings suggest that the LFA‐1/ICAM‐1 and VLA‐4/VCAM‐1 pathways are involved in leucocyte migration in both types of lung disease, while in the active phases of sarcoid

ISSN:0022-3417    

DOI:10.1002/path.1711700210

出版商:John Wiley&Sons, Ltd.    

年代:1993

数据来源: WILEY

摘要:

AbstractImmunostaining for cytokeratin has a well‐established diagnostic application in distinguishing sarcomatous mesotheliomas from sarcomas based on the premise that cytokeratin expression is common in mesotheliomas but very rare in sarcomas. However, the frequency of cytokeratin detection is highly dependent on the choice of antibody. The aim of this study was to examine the distribution of simple cytokeratins and stratified cytokeratins in 45 mesotheliomas of various types and to assess the diagnostic utility of a simple cytokeratin antibody, a stratified cytokeratin antibody, and a broad spectrum cytokeratin antibody with the aim of establishing the superiority of one for routine diagnostic use. Particular attention was paid to the potential utility of these antibodies in biopsy specimens. The broad spectrum cytokeratin antibody performed better than both the simple cytokeratin antibody (pairedt‐test:P<0.01) and the stratified cytokeratin antibody (P<0.01) as a diagnostic marker of mesothelioma and should be used in preference to the other two antibodies, particularly when considering small biopsy specim

ISSN:0022-3417    

DOI:10.1002/path.1711700211

出版商:John Wiley&Sons, Ltd.    

年代:1993

数据来源: WILEY