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PubMedDate not supplied

The development and characterization of a natural killer cell-resistant human renal cell carcinoma cell line.

Natural killer (NK) cells are large granular lymphocytes that are able to recognize and lyse a broad spectrum of transformed cells. We report one approach to identify NK surface recognition molecules on human tumor targets. A cloned renal cell carcinoma (RCC) cell line, 5117GB, sensitive to NK activity, was made NK-resistant (5117GBT) by exposure to peripheral blood mononuclear cells. Both cell lines were found to be sensitive to lymphokine-activated killer cells. Both 5117GB and 5117GBT were positive for laminin (25-33%), CD2 (LFA-3 receptor, 95-98%), CD54 (ICAM-1, 99-100%) and CD58 (LFA-3, 100%). 5117GB was positive for HLA-ABC while 5117GBT lost detectable HLA-ABC. F(ab')2 fragments of HLA-ABC were not able to block NK-mediated cytotoxicity of 5117GB. We identified 6 murine monoclonal antibodies that preferentially bind either to sensitive or resistant RCC cells. The role of each of the antigens recognized by these antibodies in NK-mediated lysis is being explored. The development of NK-sensitive and NK-resistant human solid tumor cell lines may allow further exploration of surface molecules involved with NK binding and lysis.

Antigens, Differentiation, T-Lymphocyte↗
PubMed1992

[Shedding of soluble intercellular adhesion molecule 1 (ICAM-1) from melanoma cells and the effect on cellular cytotoxicity].

ICAM-1-mediated cell-cell adhesion is essential for various immunologic functions, including non-MHC-restricted cytotoxicity. Shedding of ICAM-1 occurred after stimulation of melanoma cells with TNF alpha and IFN gamma. Soluble forms of ICAM-1 inhibited the conjugate formation of NK clones with K562 and of LAK cells with melanoma cells. Furthermore, the non-MHC-restricted cytotoxicity mediated by NK clones or LAK cells could be abrogated by soluble ICAM-1.

Cell Adhesion↗
PubMed1992

[Elevated serum levels of ICAM-1 in Wegener's granulomatosis].

Circulating soluble ICAM-1 (sICAM-1) isoforms are known to be elevated in inflammatory and autoimmune disorders (SLE, RA). A correlation between levels of circulating sICAM-1 and disease activity was described (5). In sera from 31 patients suffering from histologically confirmed Wegener's granulomatosis (WG) elevated levels of ICAM-1 were now detected in this primary systemic vasculitis. In generalized active disease circulating ICAM-1 levels were significantly higher when compared to remission and healthy control individuals. Sera from WG patients collected during intercurrent infections while on immunosuppressive drugs showed no elevation of circulating ICAM-1.

Antigens, CD↗
PubMed1992

Cellular events accompanying regression of skin recurrences of breast carcinomas treated with intralesional injections of natural interferons alpha and gamma.

Cutaneous recurrences of breast carcinomas were treated with 10 i.l. injections of nIFNs alpha and gamma delivered in combination (7 lesions) or singly (11 with nIFN-alpha, one with nIFN-gamma). Histologically confirmed complete regressions occurred in 5 of 7 lesions treated with nIFN-alpha/nIFN-gamma and in 5 of 11 recurrences injected with nIFN-alpha alone. In all cases specimens were obtained before and after therapy. In addition, in some cases (4 treated with nIFN-alpha/nIFN-gamma, 2 with nIFN-alpha, one with nIFN-gamma) multiple recurrences were injected simultaneously and were excised 24 h after 1, 3, and 10 injections and 21 days after completion of therapy. The main findings observed in the treated lesions undergoing complete and partial regressions included: (a) inhibition of mitotic activity and up-regulation of antigenic expression (mammary epithelial membrane antigen, intercellular adhesion molecule 1, HLA-DR) by the carcinoma cells; (b) activation of macrophages and dendrocytes with marked expression of HLA-DR and HLA-A,B,C; (c) infiltration of the dermis and tumors by activated T-lymphocytes (CD3+, CD4+, CD8+); (d) questionable participation by B-lymphocytes and natural killer cells; (e) activation of endothelium with enhancement of antigenic expression (intercellular adhesion molecule 1, HLA-DR), procoagulant activity, and vascular permeability. The responses elicited by nIFN-alpha/nIFN-gamma were greater than those caused by either IFN used alone. It appears that in these patients the IFNs exerted an antiproliferative action and potentiated a cell-mediated immunological response liminally present in the neoplastic tissues prior to therapy.

Administration, Cutaneous↗
PubMed1992

Differential susceptibility of cultured human melanoma cell lines to enhancement by retinoic acid of intercellular adhesion molecule 1 expression.

The potential role of intercellular adhesion molecule 1 (ICAM-1) in the biology of human melanoma cells has stimulated interest in the characterization of its modulation. The present study has shown that the differentiating agent retinoic acid (RA) up-regulates ICAM-1 expression by melanoma cells in a dose- and time-dependent fashion. The enhancement of ICAM-1 cell surface expression is paralleled by an increase in ICAM-1 mRNA. Therefore, ICAM-1 represents an additional gene which may be transcriptionally regulated by RA. The five melanoma cell lines tested displayed a differential susceptibility to the modulation of ICAM-1 expression by RA, since the cell line MeWo did not change in its ICAM-1 expression following incubation with RA. Nevertheless, RA-insensitive as well as RA-sensitive melanoma cell lines displayed a higher increase in ICAM-1 expression following incubation with RA and cytokines than following incubation with each of them. Analysis of the distribution in the melanoma cell lines of retinoic acid receptors (RARs) showed a relationship between susceptibility to a RA-mediated increase of ICAM-1 expression and RAR beta expression, suggesting that the latter receptor may play a role in the phenomenon. RAR alpha and RAR gamma were present in RA-sensitive and -insensitive melanoma cell lines, suggesting that they play a role in the enhancement by RA of cytokine-mediated up-regulation of ICAM-1 expression. The melanoma cell lines we have described may represent a useful system for investigating the role of RAR in the regulation of gene expression and the mechanism(s) which underlie this effect.

Carrier Proteins↗
PubMed1992

Human cytomegalovirus in rejected kidney grafts; detection by polymerase chain reaction.

Human cytomegalovirus (CMV) infections are frequently associated with graft rejection in the immunosuppressed patients following organ transplantation. Thirty-four tissue samples from rejected kidneys and 18 samples from normal adult kidneys obtained from autopsies were investigated for the presence of CMV-DNA by the polymerase chain reaction (PCR) and by immunohistochemistry. DNA extracted from renal tissues after proteinase K digestion was specifically amplified in 32 cycles using primers which flank a 147 bp DNA fragment of the immediate early CMV gene and analysed by slot-blot hybridization with digoxigenin-labelled detection oligonucleotides. CMV-DNA was detected by PCR in a range from 0.1 fg up to 100 fg in 14 (41%) rejected kidney transplants. Comparative immunohistological analysis revealed presence of CMV in only three biopsies of these rejected kidneys. Furthermore, CMV-DNA was also found in four of 18 (22%) normal donor kidneys. These results reveal that CMV is often present in rejected kidneys and that the infection can be transferred from the donor to the recipient, since the normal adult kidney appears to be a frequent site of latency for CMV. No differences in local immunological changes, characterized by interstitial mononuclear leukocyte infiltration as well as by aberrant expression of HLA-class II antigens and of ICAM1 on proximal tubular epithelial cells, could be detected by further immunohistological analysis between grafted kidneys at late stage of rejection with and without CMV infection.

Adolescent↗
PubMed1992

Regulation of LFA-1 avidity in human B cells. Requirements for dephosphorylation events for high avidity ICAM-1 binding.

Regulation of the avidity of LFA-1 (CD11a/CD18, alpha L beta 2) for its ligand ICAM-1 (CD54) was studied in human B cells by evaluating the effects of a phorbol ester, anti-IgM antibodies, staurosporine, and okadaic acid. We monitored changes in LFA-1 avidity by quantifying binding of cells to an immobilized rICAM-1 fusion protein. In this assay, the protein kinase C-activating phorbol ester PDB and anti-IgM antibodies, as well as the protein kinase inhibitor, staurosporine, were able to induce LFA-1-dependent binding to ICAM-1. This demonstrates that the high avidity state of LFA-1 can be induced by a protein kinase C-dependent and by a protein kinase C-independent pathway. Furthermore, treatment of the cells with the protein phosphatase inhibitor, okadaic acid, inhibited binding to ICAM-1. Treatment with staurosporine before addition of okadaic acid not only induced enhanced binding of cells to ICAM-1, but also dramatically reduced the ability of okadaic acid to inhibit binding. These results suggest a critical role for a protein phosphatase in inducing the high avidity state of LFA-1 as well as a role for a protein kinase in inducing the low avidity state of LFA-1.

Alkaloids↗
PubMedDate not supplied

Upregulation of HLA class II, but not intercellular adhesion molecule 1 (ICAM-1) by granulocyte-macrophage colony stimulating factor (GM-CSF) or interleukin-3 (IL-3) in synergy with dexamethasone.

In this study we have compared the effects of granulocyte macrophage colony stimulating factor (GM-CSF) on purified normal blood monocytes, with two other haemopoietic growth factors, Interleukin (IL-) 3 and Macrophage (M-)CSF on HLA class I, class II and intercellular adhesion molecule 1 (ICAM-1) expression in the presence and absence of dexamethasone (Dex). IL-3 alone, like GM-CSF, was a weak inducer of HLA class II expression but in combination with Dex markedly enhanced HLA-DR, DP and DQ expression. Similar changes were observed for HLA class I expression. The response to both IL-3 and GM-CSF was not additive in the presence of an optimal concentration of one cytokine and titrating concentrations of the other indicating that they may use common receptors and signal transduction mechanisms. Although IL-3 or GM-CSF alone also enhanced ICAM-1 expression, Dex inhibited both constitutive and the cytokine induced expression of this antigen. In contrast M-CSF, in the presence or absence of Dex, failed to enhance ICAM-1, HLA class I or II expression. These observations further highlight differences between the effects of the haemopoietic growth factors GM-CSF and IL-3 versus M-CSF in the regulation of monocyte function. Finally, the distinct effect of a combination of glucocorticoids with GM-CSF or IL-3 to induce high levels of HLA expression on human monocytes suggests they may have an important role during inflammatory conditions in vivo.

Cell Adhesion Molecules↗
PubMedDate not supplied

Cytokine expression and endothelial cell and lymphocyte activation in human cardiac allograft rejection: an immunohistochemical study of endomyocardial biopsy samples.

We used monoclonal antibodies and immunohistochemical staining of frozen tissue sections to study the expression of cytokines in human cardiac allograft rejection. The 113 endomyocardial biopsy samples were stained for interleukin (IL)-2, IL-6, and interferon-gamma. The findings were compared to expression of the endothelial cell adhesion molecule ICAM-1, and the lymphocyte receptor for the adhesion molecule VCAM-1, VLA-4. Four biopsy samples from patients with idiopathic cardiomyopathy served as controls. IL-2 was not expressed in lymphocytes of controls and only occasionally in mild or moderate cellular rejection, humoral rejection, and Quilty lesions. IL-2 expression was prominent in severe cellular rejection. Interferon-gamma expression increased in proportion to the severity of cellular rejection and was not expressed in other conditions. IL-6 staining, which was only observed in occasional cases, was mild. Cytokine and adhesion molecule expression tended to increase with the severity of cellular rejection. This study shows that cytokine expression can be documented in human allograft endomyocardial biopsy samples with immunohistochemical techniques. The findings support the concept of an important role for cytokines in human cardiac allograft rejection.

Antigens, CD↗
PubMed1992

Adhesion receptors are differentially expressed on developing thymocytes and epithelium in human thymus.

The thymic microenvironment consists of a network of interrelated cells of epithelial, fibroblastic, endothelial, and hemopoietic origin. Within this environment, the development of specific T-lymphocyte subpopulations partially depends on the selective interaction of T-cell precursors with such cells. Human thymic epithelial cell strains, generated with a defective retroviral vector containing simian virus 40 (SV40) large T antigen and the neomycin resistance gene or by transfection with an SV40 plasmid defective in the origin of replication, provide useful tools for understanding the mechanisms contributing to the control of T-cell maturation. Because interepithelial, epithelial-macrophage, and lymphocyte-epithelial cell interactions are important for thymocyte differentiation, the distribution of integrin and nonintegrin adhesion receptors on these cells and on developing thymocytes in vivo and in vitro has been examined in detail. Our results indicate that the transformed human thymic epithelial cell strains express the common very late antigen (VLA)-beta 1 receptor and unique alpha chains VLA-2, VLA-3, and VLA-6. The cells are also positive for LFA-3 and ICAM-1 and weakly express beta 3, beta 4, and VNR alpha. They do not express the Leu-cellular adhesion molecules (CAM). This phenotypic profile on cultured thymic epithelium generally corresponds to the distribution of integrin and other receptor molecules on thymic epithelial cells in tissue sections. The majority of thymocytes also express the integrin VLA-beta 1 and -beta 2 chains as well as VLA-4, VLA-6, and LFA-1 alpha(L). Three-color flow cytometric analyses show differential levels of expression of these adhesion receptors on human thymocyte subsets. Taken together with the immunohistochemical localization of extracellular matrix molecules, these studies suggest that both the distribution of receptor-ligand pairs and the level of expression of adhesion molecules may influence T-cell development within the thymus.

Antigens, Polyomavirus Transforming↗
PubMed1992

[Soluble intercellular adhesion molecule-I levels in sera of patients with Kawasaki disease].

We investigated whether serum levels of soluble ICAM-1 antigens increases during acute Kawasaki disease (KD). We also compared levels in acute KD with those in anaphylactoid purpura (AP) and in measles. Serum soluble ICAM-1 levels were measured by a double determinant immunoassay using two monoclonal antibodies in the FAST system. Serum levels of tumor necrosis factor-alpha (TNF-alpha) were measured by a specific and sensitive sandwich enzyme immunoassay. Patients with KD, but not with AP or measles, had increased ICAM-1 levels in serum during the acute stage. In addition, during the acute stage, KD patients with coronary-artery lesions (CAL) were found to have increased ICAM-1 levels in serum compared to patients without CAL. We found a positive correlation between serum levels of ICAM-1 and levels of TNF-alpha during acute KD. Our results suggest that the serum level of soluble ICAM-1 is an important immunologic parameter for determining the severity of vascular damage during acute KD.

Acute Disease↗
PubMed1992

The effect of Mycobacterium tuberculosis on the susceptibility of human cells to the stimulatory and toxic effects of tumour necrosis factor.

It has previously been shown that the inherently tumour necrosis factor-alpha (TNF-alpha)-sensitive L929 murine fibroblast cell line becomes much more sensitive to the cytotoxic effect of this cytokine after exposure to Mycobacterium tuberculosis in culture. In this study it is now shown that normal human cells of types likely to be involved in tuberculous lesions are affected in a similar way. Growth of normal human fibroblasts is usually stimulated by TNF-alpha in vitro, but after exposure to M. tuberculosis or to extracts of this organism, these cells are killed rather than stimulated by subsequent exposure to TNF-alpha. Similarly, human endothelial cells become susceptible to doses to TNF-alpha which do not normally affect viability. Moreover this enhancement of sensitivity to TNF-alpha is not confined to its toxicity. Endothelial cells and HeLa cells exposed to M. tuberculosis express increased levels of ICAM-1 after subsequent exposure to TNF-alpha, implying synergy between the two stimuli. It is suggested that these effects contribute to the ability of M. tuberculosis to distort the normal protective role of TNF-alpha so that the cytokine becomes detrimental to the host.

Cell Adhesion Molecules↗