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• W2079690661 abstract "Within the last several years in vivo assays have been developed to assess the biologic activities of individual cytokine gene products as antitumor agents. One such assay, termed the tumor-cytokine transplantation assay,1Tepper RI Pattengale PK Leder P Murine interleukin-4 displays potent antitumor activity in vivo.Cell. 1989; 57: 503-512Abstract Full Text PDF PubMed Scopus (759) Google Scholar, 2Tepper RI The tumor-cytokine transplantation assay and the antitumor activity of interleukin-4.Bone Marrow Transplant. 1992; 9: 177-181PubMed Google Scholar was developed to determine whether individual cytokines, when expressed locally, could incite immune and/or inflammatory cells capable of cytotoxic action against transplanted tumor cells. The assay involves the engineering of cytokine genes into expression vectors that are introduced into tumor cell lines; these modified cells are then transplanted into recipient hosts. The inhibition of growth of the cytokine-secreting tumor cells compared with mock-transfected tumor cells constitute the basis for identifying the cytokine as a potential antitumor effector. This assay has several advantages for studying the biology of cytokine-induced antitumor activity. First, it assesses the localized action of a cytokine in vivo, and therefore it recapitulates to a somewhat greater extent the normal delivery of cytokines compared with their systemic administration. Further, cytokines that can be shown to have no effect on the growth of tumor cells in vitro but that do inhibit tumor growth in vivo likely require the involvement of host effector cells in the tumoricidal effect observed. This is the case, for example, with the antitumor effect of interleukin (IL)-4.1Tepper RI Pattengale PK Leder P Murine interleukin-4 displays potent antitumor activity in vivo.Cell. 1989; 57: 503-512Abstract Full Text PDF PubMed Scopus (759) Google Scholar Histologic analysis involving routine staining methods and immunohistochemical methods can thereby provide clues to the host effector cells important in the observed antitumor response. The ability to mix tumor cells secreting cytokine with nonproducing tumor cells in a “mixed tumor transplantation assay” also allows one to assess whether the secreted cytokine is acting in a non-cell-autonomous fashion, as has been shown for a number of cytokines by this assay method. As such, the ability to test a wide spectrum of tumors of diverse histologic types for their susceptibility to the antitumor action of a given cytokine can be rapidly achieved simply by mixing individual tumor cell types with a standardized cytokine-producing cell.The tumor-cytokine transplantation assay thereby provides a means for screening in a convenient fashion, cytokines or any other gene product for in vivo antitumor activity. With this type of assay a number of cytokines have been demonstrated to possess antitumor properties in vivo. These include IL-4,1Tepper RI Pattengale PK Leder P Murine interleukin-4 displays potent antitumor activity in vivo.Cell. 1989; 57: 503-512Abstract Full Text PDF PubMed Scopus (759) Google Scholar, 3Golumbek P Lazenby A Levitsky HI et al.Treatment of established renal cancer by tumor cells engineered to secrete interleukin-4.Science. 1991; 254: 713-716Crossref PubMed Scopus (718) Google Scholar, 4Tepper RI Coffman RL Leder P An eosinophil-dependent mechanism for the antitumor effect of IL-4.Science. 1992; 257: 548-551Crossref PubMed Scopus (479) Google Scholar IL-2,5Fearon DR Pardoll DM Itaya T et al.Interleukin-2 production by tumor cells bypasses T helper function in the generation of an antitumor response.Cell. 1990; 60: 397-403Abstract Full Text PDF PubMed Scopus (945) Google Scholar, 6Gansbacher B Zier K Daniels B Cronin K Bannerji R Gilboa E Interleukin 2 gene transfer into tumor cells abrogates tumorigenicity and induces protective immunity.J Exp Med. 1990; 172: 1217-1224Crossref PubMed Scopus (666) Google Scholar, 7Bubenik J Simova J Jandlova T Immunotherapy of cancer using local administration of lymphoid cells transformed by IL-2 cDNA and constitutively producing IL-2.Immunol Lett. 1990; 23: 287-292Crossref PubMed Scopus (97) Google Scholar interferon-γ,8Watanabe Y Kuribayashi K Miyatake S et al.Exogenous expression of mouse interferon γ cDNA in mouse neuroblastoma C1300 cells results in reduced tumorigenicity by augmented anti-tumor immunity.Proc Natl Acad Sci USA. 1989; 86: 9456-9460Crossref PubMed Scopus (310) Google Scholar, 9Gansbacher B Bannerji R Daniels B Zier K Cronin K Gilboa E Retroviral vector-mediated gamma-interferon gene transfer into tumor cells generates potent and long lasting antitumor immunity.Cancer Res. 1990; 50: 7820-7825PubMed Google Scholar IL-7,10Hock H Dorsch M Diamantstein T Blankenstein T Interleukin 7 induces CD4+ T cell-dependent tumor rejection.J Exp Med. 1991; 174: 1291-1298Crossref PubMed Scopus (251) Google Scholar, 11McBride WH Thacker JD Comora S et al.Genetic modification of a murine fibrosarcoma to produce interleukin 7 stimulates host cell infiltration and tumor immunity.Cancer Res. 1992; 52: 3931-3937PubMed Google Scholar, 12Aoki T Tashiro K Miyatake S et al.Expression of murine interleukin 7 in a murine glioma cell line results in reduced tumorigenicity in vivo.Proc Natl Acad Sci USA. 1992; 89: 3850-3854Crossref PubMed Scopus (139) Google Scholar tumor necrosis factor–α (TNF-α),13Asher AI Mule JJ Kasid A et al.Murine tumor cells transduced with the gene for tumor necrosis factor-α.J Immunol. 1991; 146: 3227-3234PubMed Google Scholar, 14Teng MN Park BH Koeppen HK Tracey KJ Fendly BM Schreiber H Long-term inhibition of tumor growth by tumor necrosis factor in the absence of cachexia or T-cell immunity.Proc Natl Acad Sci USA. 1991; 88: 3535-3539Crossref PubMed Scopus (116) Google Scholar granulocyte colony-stimulating factor15Colombo MP Ferrari G Stoppacciaro A et al.Granulocyte colony-stimulating factor gene suppresses tumorigenicity of a murine adenocarcinoma in vivo.J Exp Med. 1991; 173: 889-897Crossref PubMed Scopus (310) Google Scholar and granulocyte-macrophage colony-stimulating factor.16Goillot E Tepper RL Unpublished data. 1992Google Scholar, 17Dranoff G Mulligan RC Personal communication. 1992Google Scholar Moreover, the assay has demonstrated the lack of localized antitumor activity of other cytokines such as IL-3, IL-5, and IL-10.18Wang LW Tepper RL Unpublished data. 1993Google ScholarIN VIVO ANTITUMOR ACTIVITY OF IL-4The expression of an activated murine IL-4 gene locally at the injection site of a wide variety of transplantable tumor cell types, with the previously described assay, results in a potent antitumor effect with complete killing of most tumor cell types.1Tepper RI Pattengale PK Leder P Murine interleukin-4 displays potent antitumor activity in vivo.Cell. 1989; 57: 503-512Abstract Full Text PDF PubMed Scopus (759) Google Scholar The histologic tumor types inhibited by IL-4 action in vivo include murine plasmacytomas, lymphomas, various adenocarcinomas, melanoma, and sarcomas. Moreover, human tumors, including the HT 1080 fibrosarcoma and a human glioblastoma (U87)19Yu JS Wei MX Chiocca EA Martuza RL Tepper RI Treatment of human glioma by engineered interleukin-4 secreting cells.Cancer Res. 1993; 53: 3125-3128PubMed Google Scholar are susceptible to IL-4–induced killing, as demonstrated in nu/nu mice. The action of IL-4 is clearly dose dependent, with complete eradication of tumor requiring high localized concentrations of the cytokine. For example, the degree of in vivo growth inhibition of IL-4–transfected clones of the mammary adenocarcinoma line K4851Tepper RI Pattengale PK Leder P Murine interleukin-4 displays potent antitumor activity in vivo.Cell. 1989; 57: 503-512Abstract Full Text PDF PubMed Scopus (759) Google Scholar increases with the concentration of IL-4 produced, with an eightfold reduction in tumor size in clones producing 100 U/106Gansbacher B Zier K Daniels B Cronin K Bannerji R Gilboa E Interleukin 2 gene transfer into tumor cells abrogates tumorigenicity and induces protective immunity.J Exp Med. 1990; 172: 1217-1224Crossref PubMed Scopus (666) Google Scholar cells per 24 hours compared with clones not expressing IL-4, to almost complete growth inhibition of clones expressing 3000 U of IL-4 activity. The reversal of IL-4–induced killing of tumor cells by the in vivo delivery of the neutralizing anti-IL-4 antibody 11B11 provides further evidence for the requirement of sufficient levels of IL-4 generated locally at the site of tumor cell death.1Tepper RI Pattengale PK Leder P Murine interleukin-4 displays potent antitumor activity in vivo.Cell. 1989; 57: 503-512Abstract Full Text PDF PubMed Scopus (759) Google Scholar Evidence that the action of IL-4 is not directed against the tumor cell itself is provided by the absence of an inhibitory effect of IL-4 on the growth of tumor cells in vitro and the observation that murine IL-4 can inhibit the growth of human tumor cells in nu/nu mice despite the inability of murine IL-4 to bind to the high-affinity human IL-4 receptor.20Mosley B Beckmann P March CJ et al.The murine interleukin-4 receptor: molecular cloning and characterization of secreted and membrane bound forms.Cell. 1989; 59: 335-348Abstract Full Text PDF PubMed Scopus (484) Google Scholar These findings therefore suggest a host-dependent mechanism for the antitumor effect of IL-4.The observation that the antitumor action of IL-4 is operative in T lymphocyte–deficient nu/nu mice suggests that the principal mechanism of IL-4–induced tumor cell killing is not dependent on the action of effector T cells. This finding is further supported by histologic examination of IL-4–producing tumor cells at various time points after their transplantation into syngeneic hosts. Within 48 hours IL-4–producing tumors become extensively infiltrated with host-derived granulocytes. As demonstrated by tissue Giemsa stains, more than 99% of these cells are eosinophils.1Tepper RI Pattengale PK Leder P Murine interleukin-4 displays potent antitumor activity in vivo.Cell. 1989; 57: 503-512Abstract Full Text PDF PubMed Scopus (759) Google Scholar, 4Tepper RI Coffman RL Leder P An eosinophil-dependent mechanism for the antitumor effect of IL-4.Science. 1992; 257: 548-551Crossref PubMed Scopus (479) Google Scholar Already by this time the great majority of tumor cells are killed, as evidenced by extensive tumor cell dropout, nuclear pyknosis, and absence of mitoses. Few mononuclear cells, either lymphocytes or monocytes, are observed at this point. By 96 hours eosinophil infiltration has typically declined and extensive invasion with macrophages becomes evident, but lymphocytes remain sparse. Taken together, these findings suggest that the predominant antitumor effect incited by IL-4 is a result of the activation of nonlymphoid effector cells. To define further the host cellular effector mechanism responsible for the antitumor effect of IL-4, two series of investigations were undertaken. The first involved the study of IL-4–producing tumor cells in a panel of genetically immunodeficient mouse strains. In addition to nu/nu mice, as discussed previously, bg/bg mice (natural killer [NK] cell–deficient), bg/nu/xid mice (B cell–, T cell–, and NK cell–deficient), scid mice (B cell–and T cell–deficient) and w/wv mice (mast cell–deficient) were analyzed. The antitumor activity of IL-4 could be demonstrated in each of these immunodeficient mouse strains with two different tumor types engineered to produce IL-4 (J558L plasmacytoma and B16 melanoma), providing evidence that various T-cell populations, as well as B cells, NK cells, and mast cells, are not required for IL-4–mediated tumor killing.4Tepper RI Coffman RL Leder P An eosinophil-dependent mechanism for the antitumor effect of IL-4.Science. 1992; 257: 548-551Crossref PubMed Scopus (479) Google ScholarGiven the histologic finding of eosinophil infiltration into tumors with localized IL-4 expression at the time of the bulk of tumor cell death, we sought to determine whether eosinophil depletion would inhibit the action of IL-4. The rat IgG2b monoclonal antibody RB6-8C5, which recognizes an epitope on mature myeloid cells (but not lymphocytes or monocytes) was used to achieve the in vivo depletion of eosinophils.21Pennline KJ Pellerito F DaFonseca M Monahan P Siegel MI Smith SR Flow cytometric analysis of recombinant murine GM-CSF induced changes in the distribution of specific cell populations in vivo.Cytometry. 1990; 11: 283-291Crossref PubMed Scopus (11) Google Scholar This antibody has been shown to be cytotoxic for eosinophils in vivo, resulting in the depletion of eosinophils from mice rendered hypereosinophilic by infection with the helminthic parasite Nippostrongylus brasiliensis.4Tepper RI Coffman RL Leder P An eosinophil-dependent mechanism for the antitumor effect of IL-4.Science. 1992; 257: 548-551Crossref PubMed Scopus (479) Google Scholar Neutrophils, a cell type not observed in our IL-4–induced inflammatory infiltrates, are also depleted by this antibody. With an IL-4–producing plasmacytoma cell line that fails to form tumors in vivo as a result of IL-4 expression,1Tepper RI Pattengale PK Leder P Murine interleukin-4 displays potent antitumor activity in vivo.Cell. 1989; 57: 503-512Abstract Full Text PDF PubMed Scopus (759) Google Scholar tumorigenicity could be restored in 90% of animals pretreated with RB6-8C5. Tumor formation remained inhibited in control animals receiving an irrelevant IgG antibody. Histologic analysis confirmed the depletion of eosinophils at the tumor site of animals receiving the antieosinophil antibody; viable tumor with numerous mitoses was also restored. With two other independent IL-4 tumor transfectants, RB6-8C5 antibody could be shown to synergize with anti-IL-4 antibody in the restoration of tumorigenicity. These findings suggest that an eosinophil-mediated mechanism appears to be important for the antitumor action of IL-4. The precise mechanism of IL-4–mediated tumor killing by eosinophils, however, remains to be defined. Like other granulocytes, eosinophils are known to possess phagocytic properties and can mediate killing of cellular targets by the generation of superoxide and peroxide oxygen species, and through the release, on activation, of cytotoxic granule proteins (eosinophil cationic protein, major basic protein).22Spry CJF Synthesis and secretion of eosinophil granule substances.Immunol Today. 1985; 6: 332-335Abstract Full Text PDF Scopus (34) Google Scholar Cytokines, including IL-1, TNF-α, IL-3, granulocyte-macrophage colony-stimulating factor, and tumor growth factor–β, have also been recently shown to be secreted by activated eosinophils23Galli SJ Personal communication. 1993Google Scholar, 24Moqbel R Hamid Q Ying S et al.Expression of mRNA and immunoreactivity for the granulocyte/macrophage colony-stimulating factor in activated human eosinophils.J Exp Med. 1991; 174: 749-752Crossref PubMed Scopus (165) Google Scholar, 25Kita H Ohnishi T Okubo Y Weiler D Abrams JS Gleich GJ Granulocyte/macrophage colony-stimulating factor and interleukin 3 release from human peripheral blood eosinophils and neutrophils.J Exp Med. 1991; 174: 745-748Crossref PubMed Scopus (274) Google Scholar; their action may possibly contribute to tumor cytotoxicity either by direct action, by autocrine activation of eosinophils, or by the stimulation of additional effector populations.The mechanism by which IL-4 promotes the localized eosinophil infiltration at the site of IL-4–producing tumor cells also remains to be established. The appearance of localized eosinophil infiltrates in association with IL-4 production appears to relate to a generalized type of inflammatory pattern seen with deregulated IL-4 expression in a number of naturally occurring pathophysiologic states. In patients with vernal conjunctivitis, an ocular allergic disorder, the great majority of CD4+ T-cell clones isolated from conjunctival infiltrates express IL-4 (and IL-5, but not interferon-γ) and contain large numbers of infiltrating eosinophils and mast cells.26Maggi E Biswas P DelPrete G et al.Accumulation of Th-2-like helper T cells in the conjunctiva of patients with vernal conjunctivitis.J Immunol. 1991; 146: 1169-1174PubMed Google Scholar Similarly, infection with helminthic parasites such as Schistosoma or Nippostrongylus is characterized by increased T-cell populations producing IL-4 (and IL-5) and blood, and tissue eosinophilia.27Coffman RL Seymour BWP Hudak S Jackson J Rennick D Antibody to interleukin-5 inhibits helminth-induced eosinophilia in mice.Science. 1989; 245: 308-310Crossref PubMed Scopus (539) Google Scholar Human allergic asthma is characterized by eosinophilic infiltrates in the lung, airway hyperreactivity, and lysophospholipase crystal deposition (as a result of eosinophil membrane degradation).28Robinson DS Hamid Q Ying S et al.Predominant TH2-like bronchoalveolar T-lymphocyte population in atopic asthma.N Engl J Med. 1992; 326: 298-304Crossref PubMed Scopus (2551) Google Scholar These pulmonary findings and ocular lesions resembling vernal conjunctivitis are all features of transgenic mice that we have engineered to overexpress constitutively IL-4 in T lymphocytes.29Tepper RI Levinson DA Stanger BZ Campos-Torres J Abbas AK LeDer p IL-4 induces allergic-like inflammatory disease and alters T cell development in transgenic mice.Cell. 1990; 62: 457-467Abstract Full Text PDF PubMed Scopus (348) Google Scholar Thus the proinflammatory action of IL-4 that is necessary for its antitumor activity also appears to be operative in pathophysiologic states. In both cases the action of IL-4 appears to be dependent on its localized expression at the site of inflammation.Relatively little is known about the mechanisms by which eosinophils accumulate and are activated at local sites of tissue inflammation. Previous studies have established that the adherence of human eosinophils (and basophils) to cultured human endothelial cells share some of the same functional and molecular characteristics, as does neutrophil-endothelial cell adhesion.30Pohlman TH Stanness KA Beatty PG Ochs HD Harlan JM An endothelial cell surface factor(s) induced in vitro by lipopolysaccharide, interleukin-1 and tumor necrosis factor-alpha increases neutrophil adherence by a CDw-dependent mechanism.J Immunol. 1986; 136: 4548-4553PubMed Google Scholar, 31Dobrina A Schwartz BR Carlos TM Ochs HD Beatty PG Harlan JM CD11/CD18-independent neutrophil adherence to inducible endothelial-leukocyte adhesion molecules (E-LAM) in vitro.Immunology. 1989; 67: 502-508PubMed Google Scholar Neutrophil-endothelial cell adhesion is thought to be a multistep sequential process initiated by the binding of leukocyte adhesion receptors to counterreceptors on endothelium.32Butcher EC Leukocyte-endothelial cell recognition: three (or more) steps to specificity and diversity.Cell. 1991; 67: 1033-1039Abstract Full Text PDF PubMed Scopus (2503) Google Scholar In many leukocyte types, including neutrophils, monocytes, and lymphocytes, this primary reversible adhesive event (“rolling”33von Andrian UH Chambers JD McEvoy LM Bargatze RF Arfors KE Butcher EC Two-step model of leukocyte-endothelial cell interaction in inflammation: distinct roles for LECAM-1 and the leukocyte β2 integrins in vivo.Proc Natl Acad Sci USA. 1991; 88: 7538-7542Crossref PubMed Scopus (895) Google Scholar, 34Lawrence MB Springer TA Leukocytes roll on a selectin at physiologic flow rates: distinction from and prerequisite for adhesion through integrins.Cell. 1991; 65: 859-873Abstract Full Text PDF PubMed Scopus (1872) Google Scholar ) can be mediated by the interaction of the constitutively expressed L-selectin (leukocyte–endothelial cell adhesion molecule, LAM-1, Leu-8, gp90-110 homing receptor, MEL-14 antigen) on the leukocyte surface, with the vascular E-selectin (endothelial leukocyte adhesion molecule–1 [ELAM-1]) or P-selectin (CD62) molecules on the endothelium.33von Andrian UH Chambers JD McEvoy LM Bargatze RF Arfors KE Butcher EC Two-step model of leukocyte-endothelial cell interaction in inflammation: distinct roles for LECAM-1 and the leukocyte β2 integrins in vivo.Proc Natl Acad Sci USA. 1991; 88: 7538-7542Crossref PubMed Scopus (895) Google Scholar, 35Picker LJ Warnock RA Burns AR Doerschuk CM Berg EL Butcher EC The neutrophil selectin LECAM-1 presents carbohydrate ligands to the vascular selectins ELAM-1 and GMP-140.Cell. 1991; 66: 921-933Abstract Full Text PDF PubMed Scopus (482) Google Scholar These endothelial glycoproteins are upregulated by inflammatory cytokines (such as IL-1 and TNF-α) and specifically bind to the sialylated Lewis-X lectin domain36Walz G Aruffo A Kolanus W Bevilacqua M Seed B Recognition by ELAM-1 of the sialyl determinant on myeloid and tumor cells.Science. 1990; 250: 1132-1135Crossref PubMed Scopus (882) Google Scholar of neutrophil L-selectin. Eosinophils, like other leukocytes, have also been shown to constitutively express L-selectin.37Lewinsohn DM Bargatze RF Butcher EC Leukocyte-endothelial cell recognition: evidence of a common molecular mechanism shared by neutrophils, lymphocytes, and other leukocytes.J Immunol. 1987; 138: 4313-4321PubMed Google Scholar After primary adhesion both neutrophils and eosinophils can be activated to induce or to upregulate the expression of various integrins by the process of E-selectin or P-selectin binding itself, by chemoattractant factors such as formyl-methionine–containing peptides and platelet-activating factor, and, for neutrophils, through the action of intercrine family molecules (e.g., IL-8, hMGSA/gGROα, platelet factor–4).32Butcher EC Leukocyte-endothelial cell recognition: three (or more) steps to specificity and diversity.Cell. 1991; 67: 1033-1039Abstract Full Text PDF PubMed Scopus (2503) Google Scholar Leukocyte integrin interactions with endothelial counterreceptors have been shown to promote the secondary, definitive adherence of leukocytes to the vessel wall, allowing for subsequent extravasation of inflammatory cells into the surrounding tissues.32Butcher EC Leukocyte-endothelial cell recognition: three (or more) steps to specificity and diversity.Cell. 1991; 67: 1033-1039Abstract Full Text PDF PubMed Scopus (2503) Google Scholar, 33von Andrian UH Chambers JD McEvoy LM Bargatze RF Arfors KE Butcher EC Two-step model of leukocyte-endothelial cell interaction in inflammation: distinct roles for LECAM-1 and the leukocyte β2 integrins in vivo.Proc Natl Acad Sci USA. 1991; 88: 7538-7542Crossref PubMed Scopus (895) Google Scholar, 34Lawrence MB Springer TA Leukocytes roll on a selectin at physiologic flow rates: distinction from and prerequisite for adhesion through integrins.Cell. 1991; 65: 859-873Abstract Full Text PDF PubMed Scopus (1872) Google Scholar Integrin molecules identified to participate in definitive granulocyte-endothelial adhesion include (1) the β2 (i.e., CD18-containing) integrins, such as leukocyte function associated antigen [CD11a/CD18], Mac-1, CR3 [CD11b/CD18], which bind intercellular adhesion molecule–1 (ICAM-1)34Lawrence MB Springer TA Leukocytes roll on a selectin at physiologic flow rates: distinction from and prerequisite for adhesion through integrins.Cell. 1991; 65: 859-873Abstract Full Text PDF PubMed Scopus (1872) Google Scholar on the endothelial surface; and (2) the β1 integrin, very late antigen–4 (VLA-4), which binds vascular cell adhesion molecule–1 (VCAM-1).38Elices ML Osborn L Takada Y Crouse C Luhowskyj S Lobb RR VCAM-1 on activated endothelium interacts with the leukocyte integrin VLA-4 at a site distinct from the VLA-4/fibronectin binding site.Cell. 1990; 60: 577-584Abstract Full Text PDF PubMed Scopus (1509) Google ScholarActivation of endothelial cells by cytokines such as IL-1 and TNF-α induces adherence of all granulocyte types39Bevilacqua MP Pober JS Wheeler ME Cotran RS Gimbrone MJ Interleukin 1 acts on cultured human vascular endothelium to increase the adhesion of polymorphonuclear leukocytes, monocytes, and related leukocyte cell lines.J Clin Invest. 1985; 76: 2003-2009Crossref PubMed Scopus (803) Google Scholar, 40Gamble JR Harlan JM Klebanoff SJ Vadas A Stimulation of the adherence of neutrophils to umbilical vein endothelium by human recombinant tumor necrosis factor.Proc Natl Acad Sci USA. 1985; 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144: 2558-2562PubMed Google Scholar ICAM-1,45Dustin ML Rothlein R Bhan AL Dinarello CA Springer TA Induction of IL1 and interferon-gamma: tissue distribution, biochemistry, and function of a natural adherence molecule, (ICAM-1).J Immunol. 1986; 137: 245-254PubMed Google Scholar and VCAM-1,46Osborn L Hession C Tizard R et al.Direct expression cloning of vascular cell adhesion molecule 1, a cytokine-induced endothelial protein that binds to lymphocytes.Cell. 1989; 59: 1203-1211Abstract Full Text PDF PubMed Scopus (1403) Google Scholar all of which are capable of binding eosinophils.47Weller PF Rand TH Goelz SE Chi-Rosso G Lobb RR Human eosinophil adherence to vascular endothelium mediated by binding to vascular cell adhesion molecule 1 and endothelial leukocyte adhesion molecule 1.Proc Natl Acad Sci USA. 1991; 88: 7430-7433Crossref PubMed Scopus (212) Google Scholar The transcriptional induction of VCAM-1 messenger RNA in cultured endothelial cells by IL-1 and TNF-α has been demonstrated.46Osborn L Hession C Tizard R et al.Direct expression cloning of vascular cell adhesion molecule 1, a cytokine-induced endothelial protein that binds to lymphocytes.Cell. 1989; 59: 1203-1211Abstract Full Text PDF PubMed Scopus (1403) Google Scholar IL-4 has been shown to stimulate, alone or synergistically with IL-1 or TNF-α, the upregulation of VCAM-1 on human endothelial cells, whereas ICAM-1 and ELAM-1 are unaffected by IL-4 action.48Schleimer RP Sterbinsky SA Kaiser J et al.IL-4 induces adherence of human eosinophils and basophils but not neutrophils to endothelium.J Immunol. 1992; 148: 1086-1092PubMed Google Scholar, 49Thornhill MH Wellicome SM Mahiouz DL Lanchbury JSS Kyan-Aung U Haskard DO Tumor necrosis factor combines with IL-4 or IFN-γ to selectively enhance endothelial cell adhesiveness for T cells: the contribution of vascular cell adhesion molecule-1-dependent and -independent binding mechanisms.J Immunol. 1991; 146: 592-598PubMed Google Scholar, 50Walsh GM Mermod JJ Hartnell A Kay AB Wardlaw AJ Human eosinophil, but not neutrophil, adherence to IL-1-stimulated human umbilical vascular endothelial cells is α4β1 (very late antigen-4) dependent.J Immunol. 1991; 146: 3419-3423PubMed Google Scholar Moreover, IL-4 can partially inhibit the induction of ICAM-1 and ELAM-1 by IL-1 or TNF-α in vitro,51Thornhill MH Haskard DO IL-4 regulates endothelial cell activation by IL-1, tumor necrosis factor, or IFN-γ.J Immunol. 1990; 145: 865-872PubMed Google Scholar suggesting that IL-4 may impose a selective upregulation of VCAM-1 after cytokine induction of endothelium. Monoclonal antibodies against the β2 integrins or ELAM-1 partially block the adherence of neutrophils and eosinophils in vitro52Dobrina A Menegazzi R Carlos TM et al.Mechanisms of eosinophil adherence to cultured vascular endothelial cells.J Clin Invest. 1991; 36: 20-26Crossref Scopus (249) Google Scholar; in contrast, anti-VLA-4 or anti-VCAM-1 antibodies block eosinophil adherence in vitro but have no effect on neutrophil adherence.48Schleimer RP Sterbinsky SA Kaiser J et al.IL-4 induces adherence of human eosinophils and basophils but not neutrophils to endothelium.J Immunol. 1992; 148: 1086-1092PubMed Google Scholar, 50Walsh GM Mermod JJ Hartnell A Kay AB Wardlaw AJ Human eosinophil, but not neutrophil, adherence to IL-1-stimulated human umbilical vascular endothelial cells is α4β1 (very late antigen-4) dependent.J Immunol. 1991; 146: 3419-3423PubMed Google Scholar, 52Dobrina A Menegazzi R Carlos TM et al.Mechanisms of eosinophil adherence to cultured vascular endothelial cells.J Clin Invest. 1991; 36: 20-26Crossref Scopus (249) Google Scholar This selectivity is likely explained by the fact that eosinophils but not neutrophils express the β1 integrin VLA-4.50Walsh GM Mermod JJ Hartnell A Kay AB Wardlaw AJ Human eosinophil, but not neutrophil, adherence to IL-1-stimulated human umbilical vascular endothelial cells is α4β1 (very late antigen-4) dependent.J Immunol. 1991; 146: 3419-3423PubMed Google Scholar These findings may also explain the marked impairment of neutrophil but not eosinophil or lymphocyte extravasation in patients with congenital deficiencies in CD11/CD18 expression (leukocyte adhesion deficiency syndrome).53Anderson DC Schmalsteig FC Finegold MJ et al.The severe and moderate phenotypes of heritable Mac-1, LFA-1, p150,95 deficiency: their quantitative definition and relation to leukocyte dys" @default.
• W2079690661 created "2016-06-24" @default.
• W2079690661 creator A5003952553 @default.
• W2079690661 date "1994-12-01" @default.
• W2079690661 modified "2023-10-12" @default.
• W2079690661 title "The eosinophil-mediated antitumor activity of interleukin-4" @default.
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