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A Duijvestijn

Publications and source records attributed to A Duijvestijn.

15 recordsLinked to original sources
PubMed2006

Antiendothelial cell antibodies in vasculitis and connective tissue disease.

Antiendothelial cell antibodies (AECA) are a heterogeneous family of antibodies reacting with endothelial cell antigens. These antibodies are found in various diseases and recognise several antigen determinants. Different pathophysiological effects have been observed in in vitro experiments, which include direct or indirect cytotoxicity and endothelial cell apoptosis. Furthermore, some AECA activate endothelial cells, resulting in increased leucocyte adhesiveness, activation of coagulation and vascular thrombosis. In animal models, it has been shown that AECA could promote vascular damage. Neither the endothelial cell antigens nor their precise role in the pathogenecity of different diseases in which AECA are found is well characterised. Nowadays, it is not known whether AECA are an epiphenomenon accompanying vascular injury or whether they are pathogenic. It is controversial whether fluctuations in AECA titres are associated with disease activity during follow-up studies. This review summarises the present knowledge about AECA, AECA antigens and their potential role in the pathogenecity of vasculitis and connective tissue diseases.

Animals↗
PubMed2001

Immunology and growth characteristics of ocular basal cell carcinoma.

BACKGROUND: Knowledge about immunological features and growth characteristics of palpebral (ocular) basal cell carcinomas (BCCs) is limited. In particular, it is unclear whether ocular BCC represents in this regard a special BCC entity or not. METHODS: Twenty BCCs of the lid area (ocular BCCs) were investigated immunohistologically using monoclonal antibodies against CD4, CD8, CD45Ro, CD50, CD68, HECA-452, Ki67 (MIB1), and the p53 epitope. For comparison, nine BCCs excised distant from the eye (non-ocular BCCs) were evaluated. RESULTS: In BCCs the distribution of the immunocompetent cells investigated is markedly irregular. These cells are localized mainly around BCC islands. Only a few of them invade tumour cell aggregates. The CD4:CD8 ratio as detected by immunohistochemistry is >1 in 82% of ocular BCCs and in 88% of nonocular BCCs. Often there are dense infiltrations of CD68+ cells (macrophages) and HECA-452+ cells adjacent to tumour cell aggregates. The growth fraction [percentage of proliferating (Ki67+/MIB 1+) cells] varies from 0% to more than 30%. Proliferative activity is enhanced at the invasion front. Additionally, the amount of p53+ cells differs considerably among the BCCs. CONCLUSIONS: CD4+ T cells seem to be the most important cell population for BCC immunosurveillance, offering the chance for conservative interferon therapy. The role of CD68+ and HECA-452+ cells has to be further elucidated. In many tumours the large amount of proliferating cells contrasts to the usually slow growth of BCCs, indicating strong apoptotic processes. The results can be regarded only as semiquantitative. So far, ocular and nonocular BCCs exhibit no essential differences regarding immunocompetent cell infiltration and growth characteristics. According to this, palpebral BCCs are "normal" BCCs and not a special BCC variant. Therefore, results from dermatological research concerning BCC can be extended without limitations to their counterparts in the lid area.

Adult↗
PubMed1999

[High endothelial venules. Kinetics of the expression in IRBP-induced experimental autoimmune uveitis].

UNLABELLED: Experimental autoimmune uveitis (EAU) is a T-cell-mediated disease expressing high endothelial venules (HEVs) in the retina. HEVs could be responsible for the absorption of activated T-cells. The purpose of this study was to investigate the kinetics of HEV expression in the murine IRBP (interphotoreceptor retinoid binding protein) induced EAU. METHODS: B10. A mice were immunized subcutaneously with IRBP. The eyes were analysed on days 10, 18, 24 and 28 (n = 5 for each time point). While HEVs were identified with the mAb MECA 325, the control mAb MECA 20 stained all endothelial cells. RESULTS: HEVs were detectable in the intact retina from day 10. Presence of HEVs peaked on day 18 and decreased by day 28, when maximal inflammation and retinal destruction was detectable. CONCLUSION: HEV expression could play a central role in the onset of EAU, allowing homing and migration of inflammatory cells into the eye.

Animals↗
PubMed1992

Chronic renal allograft rejection: the significance of non-MHC alloantigens.

We studied the role of polymorphic endothelial antigens other than MHC in antibody-mediated chronic renal allograft rejection in two models. In the first model, donor Lewis rat kidneys were transplanted into BN recipients that had been made tolerant for donor class I antigens at the B cell (antibody) level. In this setting Lewis kidney grafts were chronically rejected with stable renal function but increasing proteinuria (> 100 mg/24 h). Rejected graft tissue showed mononuclear cell infiltration and the presence of glomerular vasculonecrotic lesions with fibrinoid material, associated with IgG and IgM deposition, but with absent or weak C3 binding. Graft endothelium showed no expression of MHC class II antigens. Serum antibodies were not reactive with donor class I antigens, but did react with endothelial non-MHC alloantigens. In the second model, more direct information on the role of endothelial non-MHC alloantigens in renal allograft rejection was obtained by transplanting Lewis 1 N kidneys into unmodified BN recipients (MHC-matched transplants). Here, similar to the first model, the animals developed severe proteinuria with stable renal function. Histopathological examination showed mononuclear cell infiltration and deposition of IgM and IgG along the glomerular vasculature, but this time in the presence of strong C3 reactivity. However, glomerular vasculonecrotic lesions with intense fibrin deposition were not observed. The data showed that although clinically the two kidney transplantation models used gave similar chronic rejection phenomena, histopathologically some striking differences were observed in the glomeruli. The precise mechanisms effecting chronic rejection of the grafts is still a puzzle. However, immune reactivity against graft (endothelial) non-MHC antigens may play a significant role.

Animals↗
PubMed1991

Dissection of murine lymphocyte-endothelial cell interaction mechanisms by SV-40-transformed mouse endothelial cell lines: novel mechanisms mediating basal binding, and alpha 4-integrin-dependent cytokine-induced adhesion.

Lymph node-derived endothelial cells were immortalized by infection with SV40 virus and subclones expressing the marker MECA 325 specific for high-endothelial venules (HEV) were selected. These transformed mouse endothelial (TME-) cell lines grow permanently without requirement for special growth factors. Staining of the selected clones with endothelium-specific antibodies and with anti-von Willebrand factor antiserum and uptake of acetylated low-density lipoprotein provide evidence for their endothelial origin. The vascular addressins identified by mAbs MECA 79 and MECA 367 on HEV are not detectable, indicating that the phenotype of the cells differs from that of HEV-type endothelium. The TME cells display a constitutive capacity to bind lymphocytes. An additional binding component is induced by treatment of the TME cells with TNF alpha. Antibodies against the homing receptor LECAM-1 (lectin-related leucocyte-endothelial cell adhesion molecule 1), alpha 4-integrins, vascular addressins, LFA-1, or ICAM-1 known to block lymphocyte interaction with particular types of HEV were unable to inhibit the basal adhesion to TME cells, indicating that a further binding mechanism in mice is displayed by this cell type. The adhesion component induced by TNF alpha is mediated by alpha 4-integrins since enhanced binding could be blocked by an antibody against mouse alpha 4 (lymphocyte-Peyer's patch adhesion molecule 1/2). TME cell lines therefore seem to be a useful model for the dissection and analysis of hitherto poorly characterized murine lymphocyte/endothelial cell interaction mechanisms.

Animals↗
PubMed1989

Lymphocyte homing receptors and adhesion molecules in intravascular malignant lymphomatosis.

Intravascular malignant lymphomatosis (IML) is a highly malignant, recently recognized form of lymphoma. It is characterized by multifocal proliferation of malignant lymphocytes within small blood vessels, primarily in the central nervous system and skin, frequently resulting in circulatory disturbances. The cause of the impaired capability of the malignant lymphocytes to extravasate has remained unclear. We analyzed the presence of immunoreactivity for certain homing receptor and adhesion molecules associated with lymphocyte extravasation in 3 patients with this disease. Compared with non-neoplastic leukocytes, large malignant lymphocytes appeared either negative or only weakly positive for the leukocyte surface glycoprotein, CD18 that is the beta chain of the CDIIa/CD18 complex (lymphocyte-function associated antigen-I, LFA-I), which mediates cell-to-cell adhesion of lymphocytes. On the other hand, antibody to one of the proposed ligands for this complex, intercellular adhesion molecule-I, gave positive reactivity both on lymphocytes and on endothelial cells. Further, the malignant lymphoid cells stained positively with Hermes-3 antibody, which recognizes a common structure of CD44 class of molecules involved in lymphocyte homing. It was also shown that HECA-452 antigen, a marker of high endothelial venules (HEV) supporting lymphocyte extravasation, can be synthesized by an IML patient even at the site of inflammation but it is not prerequisite for extravasation of inflammatory lymphocytes. Our results suggest that the deficiency or absence of the adhesion molecule CDIIa/CD18 may contribute to the inability of the malignant lymphoid cells to extravasate in IML, and perhaps also to the high malignancy of this form of lymphoma.

Aged↗
PubMed1989

Mechanisms and regulation of lymphocyte migration.

Lymphocyte traffic seems to be an essential requirement for an adequate immune response both in lymphoid tissues and local inflammatory sites. In this review, Adrian Duijvestijn and Alf Hamann discuss how selective migration of lymphocytes is directed by lymphocyte-endothelial interactions and what mechanisms may control this.

Animals↗
PubMed1988

Evidence for an accessory role of LFA-1 in lymphocyte-high endothelium interaction during homing.

In a variety of lymphocyte interactions, lymphocyte function-associated antigen-1 (LFA-1) plays an important role as an accessory mechanism mediating cell adhesion. We tested the possibility that LFA-1 could also be involved in the specific binding of lymphocytes to high endothelial venules (HEV) during homing. Antibodies against LFA-1 but not against various other cell surface molecules (except the putative gp90 homing receptor defined by the MEL-14 antibody) were found to inhibit in vitro adherence of lymphocytes to HEV in frozen sections of lymph nodes. Binding of T cell lines to HEV was also inhibited by anti-LFA-1 antibody. Using sublines selected for differential expression of the MEL-14 antigen, MEL-14 high cells (which bind well to HEV) were less susceptible to inhibition by anti-LFA-1 than poor binders with low levels of the homing receptor, supporting the model of LFA-1 being an accessory mechanism strengthening weak interactions between cells. Parallel results were found in vivo where anti-LFA-1 antibodies reduced the migration of normal lymphocytes into lymph nodes and Peyer's patches by 40 to 60%. Localization in the lung, especially of activated lymphocytes, was also impaired, although to a lesser extent. These findings suggest that LFA-1 plays an accessory role in cellular interactions relevant for lymphocyte migration.

Animals↗
PubMed1988

Regulation of lymphocyte homing. I. Alterations in homing receptor expression and organ-specific high endothelial venule binding of lymphocytes upon activation.

Upon activation, lymphocytes display profound alterations in their in vivo migration behavior. In an attempt to understand some of the cellular mechanisms responsible for this altered behavior, in vitro stimulated lymphocytes have been analyzed for their expression of a putative homing receptor (HOR) (defined by mAb MEL-14) and for their ability to bind to specialized lymphoid organ high endothelial venules (HEV) in vitro. The results indicate that signals related to lymphocyte activation induce complex alterations in HOR expression and organ-specificity of HEV-binding: 1) submitogenic stimuli induce an increase in MEL-14 antigen expression. This applies to almost all lymphocytes in autologous cultures, for the fraction of cells in periodate, LPS- or Con A-treated cultures not fully activated and for cultures stimulated with suboptimal doses of Con A. 2) Full blast transformation is associated with a decrease or complete loss of MEL-14 antigen expression on the majority of blasts in all activating systems used, but a subset of up to 30 to 40% of fully activated cells may nonetheless express very high levels of the MEL-14 antigen. 3) Functional assays reveal that Con A and periodate stimulation lead to a selective, nearly complete suppression of the lymphocytes binding to HEV of Peyer's patches, even under conditions where overall binding to peripheral node HEV is increased. This indicates a differential regulation of the two respective receptors, with the mucosa system-specific HOR being more prone to down-regulation during in vitro activation by these mitogens.

Animals↗
PubMed1986

Interactions between endothelial cells and leukocytes.

We present evidence that specific receptors are utilized by neutrophils to control their interaction with endothelial cells at sites of acute inflammation and that these receptors are related if not identical to lymphocyte "homing receptors" for lymphoid tissue high endothelium. We speculate that such receptors play a fundamental but not exclusive role in controlling the extravasation and tissue localization of all bone marrow-derived nucleated cells. In addition, we emphasize the active role of endothelial cells in the process of lymphocyte migration and leukocyte extravasation. By the expression of as yet unidentified organ-specific determinants for lymphocyte recognition, endothelial cells control the exit of particular lymphocyte subsets into mucosal versus nonmucosal sites, thus helping to determine the unique features of mucosal versus nonmucosal immune responses. Furthermore, we argue that endothelial cells are exquisitely responsive to local immune reactivity and present evidence that specific lymphokines, including gamma-interferon, play an important role in inducing postcapillary venules to express differentiated features required for the support of lymphocyte traffic into lymphoid organs and into sites of chronic inflammation. Leukocytes, endothelial cells, and probably other tissue cell classes appear to interact at multiple levels by a variety of mechanisms to regulate the local extravasation of immune effector cells.

Animals↗
PubMed1983

Large mononuclear Ia-positive veiled cells in Peyer's patches. I. Isolation and characterization in rat, guinea-pig and pig.

The antigen presenting cell system in the skin is extensively studied, and is supposed to consist of Langerhans cells in epidermis and dermis, veiled cells in skin lymph and interdigitating cells in skin lymph nodes. In order to detect whether a similar cell system is present in the gut, we studied Peyer's patch cell suspensions. Mononuclear cells with long actively moving cytoplasmic veils were found in cell suspensions from Peyer's patches of rat, guinea-pig, and pig, and in cell suspensions from small intestinal villi of guinea-pig and pig, but not of rat. These veiled cells are strongly Ia-positive. Because of their Ia positivity, their enzyme cytochemical staining pattern, and their ultrastructure, these cells resemble the antigen presenting cells of the skin, skin lymph and lymph node.

Animals↗