Kaposi's sarcoma-associated herpesvirus/human herpesvirus 8 is not detectable in peripheral blood mononuclear cells of the relatives of sporadic KS patients.
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Adult↗
Biomedical subjects
S Uccini
Publications and source records attributed to S Uccini.
Kaposi's sarcoma cells express the macrophage-associated antigen mannose receptor and develop in peripheral blood cultures of Kaposi's sarcoma patients.
The mannose receptor (MR) is a surface 175-kd C-type lectin expressed by macrophages and dendritic cells. MR is involved in removal of effete cells, phagocytosis of mannose-coated particles, pinocytosis, and antigen presentation. Expression of MR was investigated in 17 biopsies of Kaposi's sarcoma (3 AIDS KS, 13 classical KS, and 1 transplant-associated KS) using three anti-MR monoclonal antibodies (3.29, D547, and PAM1). Immunostaining for MR was detected in 94 +/- 7% KS cells with spindle morphology. In normal tissues, MR was expressed by sinus-lining cells of spleen and lymph nodes, but it was not detected in endothelial cells lining normal hematic and lymphatic vessels, hemangioma, hemangioendothelioma, and lymphangioma. Expression of MR in KS cells prompted us to investigate the possibility that they derive from a circulating precursor cell. Peripheral blood mononuclear cells from 16 patients with KS (10 classical, 1 transplanted, and 5 AIDS) were cultured in PHA-conditioned medium for 10 to 14 days. Confluent monolayers of adherent spindle cells were detected in 8 of 11 classical KS, in 5 of 5 AIDS KS patients, and in 0 of 34 control patients. Peripheral-blood-derived KS-like cells were characterized by co-expression of macrophage and endothelial antigens being positive for CD45 (60%), CD68 (98%), MR (70%), CD14 (25%), VE-cadherin (70%), and von Willebrand factor (10%). When the immunophenotype of peripheral-blood-derived adherent cells was compared with that of KS spindle cells of tissue biopsies, it was found that both cell types are VE-cadherin+/MR+/CD68+, that peripheral-blood-derived spindle cells are CD34- and are less frequently stained for CD31 and von Willebrand factor, and that lesional KS cells do not express the leukocyte markers CD45 and CD18. Our findings are consistent with the possibility that KS lesions derive from tissue accumulation and local proliferation of a special subset of macrophages with endothelial features the normal counterpart of which are the sinus-lining cells of spleen and lymph nodes.
Acquired Immunodeficiency Syndrome↗
Arteriomegaly and inflammatory abdominal aortic aneurysm. Case report.
In this case report inflammatory abdominal aortic aneurysm (IAAA) was superimposed on an arteriomegaly condition complicated by bilateral aneurysm of the common iliac arteries. Obstruction of the right ureter, mild hydronephrosis of the left system and a slight impairment of renal function were also present. Preoperative cellular and humoral immunological parameters were within normal limits while the erythrocyte sedimentation rate (ESR) was elevated (74 mm). Histological analysis showed numerous scattered lymphoid cells or organized in follicles with germinal centers within the adventitial thickening of the IAAA wall. Immunohistochemical analysis on frozen sections demonstrated that dispersed and perivascular lymphoid cells were mainly composed of similar amounts of CD3+/CD4+ and CD3+/CD8+ T lymphocytes. Histological analysis of the common iliac artery aneurysm showed a mild intimal thickening will small aggregates of macrophages. After aneurysm repair all peripheral blood analysis normalized within one month after surgery. The IAAA observed in our patient with arteriomegaly as underlying arterial disease cannot be interpreted as an inflammatory variation of an atherosclerotic aneurysm. The histological pattern of the inflammatory reaction and its resolution after surgery give, in our opinion, more credit to the etiopathogenetic hypothesis of a reaction elicited by an antigen within the arterial wall of the infrarenal aorta which might be enhanced by the lymphatic stasis subsequent to aneurysm compression.
Aged↗
[HIV-1 virus uses a double-key mechanism to infect the cell].
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Binding, Competitive↗
Expression of ICAM-1 and VCAM-1 in human malignant mesothelioma.
Intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) are cytokine-inducible adhesion molecules which recognize ligands that are highly expressed on leukocytes. Expression of ICAM-1 and VCAM-1 was investigated in tissue sections of 16 cases of malignant mesothelioma (seven epithelial, eight biphasic, and one sarcomatoid) using immunohistochemistry. Neoplastic cells were diffusely and intensely stained for ICAM-1 in all cases. VCAM-1 was detected in 14 of 16 cases. The percentage of VCAM-1-positive tumour cells was more than 50 per cent in eight cases and the staining was observed mainly in epithelial-like cells. VCAM-1 was rarely expressed in other malignant tumours of epithelial origin, being present in only 1 of 58 cases of carcinoma originating from different anatomical sites. At the cellular level, ICAM-1 and VCAM-1 appeared co-distributed, the staining for both being cytoplasmic with a membrane reinforcement. The regulation of VCAM-1 expression by neoplastic mesothelial cells was investigated in vitro using 14 mesothelioma cell lines. ICAM-1 was expressed by cultured cells of all mesothelioma cell lines, even in the absence of cytokines. VCAM-1 was detected in 10-50 per cent of the cells in three non-stimulated mesothelioma cell lines (mero-95, mero-96, and mero-134), and was absent or poorly expressed in the remaining 11. Exposure of a negative cell line (mero-48a) to an optimal concentration of tumour necrosis factor alpha (TNF alpha) or interleukin-13 (IL-13) for 6-18 h resulted in the induction of VCAM-1 mRNA synthesis and in VCAM-1 expression at the membrane level in 60-70 per cent of the cells. These findings are consistent with the possibility that TNF alpha, IL-13, or other activating signals are released in the tumour micro-environment and regulate the expression of VCAM-1 in malignant mesothelioma cells.
Blotting, Northern↗
Comparison of the Vbeta repertoire in peripheral blood and in lymph nodes of HIV-infected subjects reveals skewed usage predominantly in CD8+ T cells.
Perturbations of the repertoire of variable-beta (Vbeta) regions of the T cell receptor have been observed in patients infected by HIV and have been attributed to stimulation by viral antigens or superantigens. We further sought for traces of HIV-induced perturbations by comparing Vbeta repertoire in peripheral blood and in lymphoid tissues of six infected patients. Vbeta expression was studied with a panel of 17 anti-Vbeta antibodies covering about 50% of the entire repertoire. We observed major divergences between lymph nodes and peripheral blood in the expression of several Vbeta segments, and these differences were significantly more frequent in CD8+ than in CD4+ T cells (P = 0.0097). Vbeta2 was perturbed in CD8 cells from all but one patient. One HIV-negative subject with localized reactive lymphadenopathy of unknown etiology had four perturbed Vbeta segments, including Vbeta2, in CD8+ cells, while another uninfected subject with an unreactive lymph node architecture had no perturbations. Our findings suggest that stimulation by HIV or by other antigens determines divergences in the Vbeta repertoire between lymphoid tissues and peripheral blood predominantly in CD8+ T cells.
Adult↗
Plasma HIV viremia and viral load in lymph nodes.
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Acquired Immunodeficiency Syndrome↗
Expression of adhesion molecules and extracellular matrix proteins in glioblastomas: relation to angiogenesis and spread.
We studied the immunohistochemical expression of inducible adhesion molecules, integrins and extracellular matrix proteins in 10 cases of glioblastoma multiforme in order to investigate their angiogenesis, local invasiveness, poor metastasizing properties and their lack of tumour infiltrating leukocytes. In glioblastomas endothelial proliferations represent the majority of vascular structures; they were positive for endothelial markers (vWF, CD31, VE-cadherin) and negative for macrophage markers (CD68, PAM-1). Immunohistologically, they were subtyped into: 1 solid-glomeruloid ICAM-1, alpha 2 beta 1, alpha 3 beta 1, alpha 5 beta 1 negative; 2 channelled-branching ICAM-1 negative and alpha 2 beta 1, alpha 3 beta 1, alpha 5 beta 1 positive; 3 channelled-telangiectatic ICAM-1, alpha 2 beta 1, alpha 3 beta 1, alpha 5 beta 1 positive. In channelled proliferations, the expression and distribution of tenascin and merosin in the basal membrane was similar to that of normal brain vessels. The expression of all these molecules might indicate different steps of maturation of endothelial proliferations. The majority of endothelial proliferations may be immunohistologically considered as incomplete vascular structures; this might account for the low metastasizing tendency and low recruitment of leukocytes by these tumours. Neoplastic astrocytes were GFAP-1, ICAM-1, VCAM-1, alpha 2 beta 1, alpha 3 beta 1 and alpha 5 beta 1 immunoreactive and alpha 6 beta 4 negative: this allows them to interact with extracellular matrix proteins and might, in part, explain the tendency of glioblastomas to infiltrate locally.
Brain Neoplasms↗
[Undifferentiated carcinoma of the rhinopharynx: an immunohistochemical study of adhesion molecules].
CU-NPC is an important clinical entity that presents some uncertainties regarding histologic features. In fact many of these tumors show a marked infiltration of lymphocytes justifying the term "lymphoepithelioma" used to define these tumors in the past. Although they have not yet been placed in a definite category, some factors may be responsible for the lymphocyte infiltration; infection by Epstein-Barr virus, expression by tumor cells of HLA-DR antigens and intercellular adhesion molecules (ICAM-1) and production of interleukin l-alpha by U-NPC derived cell lines. A recent study showed that epithelium of the crypts of the tonsils exerts an active role in the intraepithelial migration of lymphocytes. This recruitment from the underlying lymphatic tissue could be determined by the expression, on the part of the basal cells of tonsillar crypts, of ICAM-1 and blood vessel adhesion molecules (VCAM-1). The purpose of this study was to verify the presence of ICAM-1 and VCAM-1 in paraffin-embedded tissue section of seven cases of U-NPC. The results showed positive immunohistochemical reaction both for ICAM-1 and VCAM-1. On this basis, the authors hypothesize that the expression of these molecules could favor intratumoral recruitment of lymphocytes similar to what occurs in the epithelium of the tonsillar crypts.
Carcinoma↗
Expression of VE (vascular endothelial)-cadherin and other endothelial-specific markers in haemangiomas.
Haemangiomas are vascular tumours characterized by rapid growth and increased endothelial turnover. VE-cadherin is a recently discovered endothelial cell-specific cadherin located at intercellular junctions. In different types of epithelial tumours, cadherin expression is inversely correlated with invasiveness and metastatic dissemination. In this immunohistochemical study, VE-cadherin expression has been analysed in different types of haemangioma. VE-cadherin is highly expressed in endothelial cells of haemangiomas and is decreased, but still detectable, in some cases of haemangionendothelioma and angiosarcoma. The antigenic profile of most haemangioma cells was similar to that of normal endothelium. CD31, CD34, ICAM-1, von Willebrand factor, and VLA integrins were expressed in haemangioma endothelium; in addition, the major components of vascular basement membrane, namely fibronectin, collagen type IV, and laminin, were correctly expressed and organized. Surprisingly, a marked reactivity for the M form of laminin (merosin) was detected in the basement membranes of two juvenile capillary haemangiomas. Overall, this study shows that, with the exception of angiosarcoma and haemangionendothelioma, vascular tumours maintain most of the differentiation characteristics of normal endothelium. This encourages speculation that in these pathologies, abnormal endothelial proliferation is more related to the release of local factors than to an altered endothelial phenotype.
Basement Membrane↗
The lymphoepithelial organization of the tonsil: an immunohistochemical study in chronic recurrent tonsillitis.
Interactions between leukocytes and crypt epithelium were extensively investigated in 12 cases of chronic recurrent tonsillitis, using immunohistochemistry and cytofluorimetric analysis of cell suspensions. Intraepithelial leukocytes are a mixed cell population composed of 50 per cent CD20-positive B lymphocytes, 40 per cent T lymphocytes with a 2.7 CD4/CD8 ratio, and 10 per cent CD68-positive macrophages. About 4 per cent of intraepithelial leukocytes are proliferating cells, as indicated by Ki-67 staining. Leukocyte infiltration is associated with expression on epithelial cells of the adhesion molecules ICAM-1 and VCAM-1. Crypt epithelium is supported by a basement membrane showing frequent interruptions and connected with the reticular stroma of the lymphoid tissue, which was stained for fibronectin, tenascin, collagen, and laminin. Extracellular matrix (ECM) distribution was correlated with integrin expression on B and T lymphocytes. It was found that the ECM was arranged differently in the follicles and in the extrafollicular area and that B and T lymphocytes exhibited different patterns of integrin expression.
Adolescent↗
Low expression of E-selectin in diseased tissues from human immunodeficiency virus-positive patients.
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Blood Vessels↗
Co-expression of endothelial cell and macrophage antigens in Kaposi's sarcoma cells.
The histopathogenesis of Kaposi's sarcoma (KS) was investigated using immunocytochemistry in 12 skin biopsies obtained from two AIDS patients, nine patients with the classic form, and one organ-transplant patient. KS cells revealed a peculiar antigenic profile, being characterized by co-expression of endothelial and macrophage markers. KS cells were stained for von Willebrand factor (vWF); for vascular endothelial (VE) cadherin, an endothelial specific adhesion molecule; and for PECAM/CD31. In addition, they expressed the macrophage antigens PAM-1, CD68, and CD14, and were positive for vitronectin receptor and alpha-1,5,6/beta-1 integrins. KS cells were weakly stained for ICAM-1 in 6 of 12 cases and were negative for VCAM-1 and E-selectin.
Acquired Immunodeficiency Syndrome↗
Expression of intercellular adhesion molecule-1 and vascular cell adhesion molecule-1 in undifferentiated nasopharyngeal carcinoma (lymphoepithelioma) and in malignant epithelial tumors.
Immunoreactivity for intercellular adhesion molecule-1 (ICAM-1) and for vascular cell adhesion molecule-1 (VCAM-1), two adhesion molecules of the immunoglobulin (Ig) superfamily, was tested and measured on tissue sections from 16 undifferentiated nasopharyngeal carcinomas (U-NPC), 12 keratinizing squamous cell carcinomas (SCCs) of the head and neck region, and 54 malignant epithelial tumors of various origin. Neoplastic cells of all cases of U-NPC were diffusely and intensely stained for ICAM-1 and VCAM-1. Moreover, ICAM-1 messenger RNA (mRNA) and VCAM-1 mRNA were detected by Northern blot analysis of RNA extracts from two tumors. In the other epithelial tumors focal or diffuse staining for ICAM-1 was observed in 40 cases (66%), whereas reactivity for VCAM-1 was detected in a single case of metastatic undifferentiated carcinoma of unknown origin. The biopsy specimens of U-NPC showed variable infiltration by leukocytes, which were positive for the integrins lymphocyte function antigen-1 (LFA-1) and alpha-4/beta-1, the corresponding ligands for ICAM-1 and VCAM-1. The possibility that ICAM-1 and VCAM-1 on neoplastic cells may favor the intratumoral recruitment of leukocytes in a way similar to that occurring in crypt epithelium of the palatine tonsil is discussed.
Adolescent↗
Incidence and clinic-pathologic features of non-Hodgkin lymphoma in a cohort of human immunodeficiency virus positive coagulopathic patients.
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Blood Coagulation Disorders↗
Subtypes of Epstein-Barr virus in HIV-1-associated and HIV-1-unrelated Hodgkin's disease cases.
Epstein-Barr virus (EBV) type 2 is considered to be a much less potent transformer of lymphocytes than type 1. However, type-2 EBV may be involved in the pathogenesis of non-Hodgkin's lymphomas (NHLs) arising in immunocompromised patients, i.e., subjects with malaria or HIV-1 infection. To determine whether type-2 EBV may also play a role in Hodgkin's disease (HD) developing in immunocompromised patients, we characterized EBV subtypes in EBV-positive HD samples from 10 HIV-1-positive patients as well as from a control population of 24 HIV-1-negative patients. Type-2 EBV was detected in 5/10 HD samples from the HIV-1-positive group (1 case showed concomitant type-1 EBV positivity), but only in 1/20 HD samples from the HIV-1-negative group, indicating that, during HIV-1-induced immunodepression, type-2 EBV may be pathogenetically involved also in HD, as previously reported for HIV-associated NHLs.
Base Sequence↗
Molecular mechanisms involved in intraepithelial lymphocyte migration: a comparative study in skin and tonsil.
Intraepithelial lymphocyte migration is a biological process frequently observed in skin and tonsil. Using immunohistochemistry, we have studied the molecular bases of this process in seven skin biopsies involved by mycosis fungoides (MF) and in 12 tonsils, four involved by B-chronic lymphocytic leukaemia (B-CLL) and eight by lymphoid follicular hyperplasia (LH). In the skin, intraepidermal T-lymphocyte infiltration was associated with narrowing and fragmentation of the basement membrane, as shown by an anti-collagen type IV antibody. Immunostaining of serial sections with an anti-collagenase type IV antibody revealed that collagenase type IV was localized in the upper dermis and strictly co-distributed with collagen type IV, suggesting that enzymatic digestion played a role in the alterations of the basement membrane. Further migration through the epidermis was mediated by expression on keratinocytes of intercellular adhesion molecule-1 (ICAM-1) and of leukocyte-function associated antigen-1 (LFA-1) on infiltrating lymphocytes. In the tonsil, intraepithelial infiltration was mediated by the expression of vascular cell adhesion molecule-1 (VCAM-1) by epithelial cells and of very late antigen-4 (VLA-4) by infiltrating lymphocytes. Further intraepithelial lymphocyte migration was then established, as already shown in the skin, by ICAM-1/LFA-1 interaction. Lymphocyte recruitment from the systemic circulation was studied using antibodies directed against endothelial leukocyte adhesion molecule-1 (ELAM-1), ICAM-1, and VCAM-1. These adhesion molecules were highly expressed by blood vessels in the upper dermis of MF and the percentage of ELAM-1+/VCAM-1+ vessels was significantly higher than that observed in tonsils.(ABSTRACT TRUNCATED AT 250 WORDS)
Basement Membrane↗
Expression and modulation of a mononuclear phagocyte differentiation antigen (PAM-1) during in vitro maturation of peripheral blood monocytes.
Human macrophages obtained by in vitro maturation of peripheral blood monocytes express a surface antigen, PAM-1, recognized by a monoclonal antibody and typical of pulmonary alveolar and tissue macrophages. PAM-1, undetectable in freshly isolated peripheral blood monocytes, was expressed in monocyte-derived macrophages after 3 days of in vitro adherent culture and was maximal after 14-15 days (50%-60% of positive cells). Similar levels of PAM-1 positivity were observed in non-adherent monocyte-derived macrophages suggesting that cell adhesion was not a critical requisite for the expression of this antigen. Bacterial lipopolysaccharide and a monocyte chemotactic protein preparation respectively suppressed and upregulated PAM-1 expression in monocyte-derived macrophages. In contrast, interferon-gamma, although enhancing the levels of class II HLA-DR antigen in monocyte-derived macrophages, did not influence the kinetics of appearance and the levels of PAM-1 in these cells. Thus, expression of PAM-1, which is restricted to certain stages of the monocyte-macrophage differentiation pathway, is also differentially modulated by activation signals, which can be present in the micro-environment of inflammed tissues.
Antigens, Differentiation↗