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9. The x-linked lymphoproliferative-disease gene product SAP regulates signals induced through the co-receptor SLAM

Author

Sayos, J., Wu, C., Morra, M., Wang, N., Zhang, x., Allen, D., van Schaik, S., Notarangelo, L., Geha, R., Roncarolo, M.G., Oettgen, H., De Vries, J.E., Aversa, G., and Terhorst, C.

Subjects
Epstein-Barr virus diseases -- Research, Lymphocytes -- Observations, Antigen receptors, T cell -- Observations, Environmental issues, Science and technology, Zoology and wildlife conservation
Abstract

Signalling lymphocyte-activation molecule (SLAM) is a glycosylated type-I transmembrane protein present on the surface of B and T cells. It is shown that a T-cell specific SLAM associated protein (SAP), containing an SH2 domain and a short tail, blocks recruitment of the SH2-domain containing signal transduction molecule SHP-2 to a SLAM cytoplasmic region docking site. Absence of the SAP inhibitor in XLP patients has an effect on T/B cell interactions, resulting in inability to control B-cell proliferation caused by Epstein-Barr viruses.

Published
1998

11. Clinical Experience with L-Asparaginase

Author

Oettgen, H. F., Tallal, Lisa, Tan, Charlotte C., Murphy, M. L., Clarkson, B. D., Golbey, R. D., Krakoff, I. H., Karnofsky, D. A., Burchenal, J. H., Allfrey, V. G., editor, Allgöwer, M., editor, Bauer, K. H., editor, Berenblum, I., editor, Bergel, F., editor, Bernard, J., editor, Bernhard, W., editor, Blokhin, N. N., editor, Bock, H. E., editor, Bucalossi, P., editor, Chaklin, A. V., editor, Chorazy, M., editor, Cunningham, G. J., editor, Dameshek, W., editor, Dargent, M., editor, Della Porta, G., editor, Denoix, P., editor, Dulbecco, R., editor, Eagle, H., editor, Eker, R., editor, Grabar, P., editor, Hamperl, H., editor, Harris, R. J. C., editor, Hecker, E., editor, Herbeuval, R., editor, Higginson, J., editor, Hueper, W. C., editor, Isliker, H., editor, Karnofsky, D. A., editor, Kieler, J., editor, Klein, G., editor, Koprowski, H., editor, Koss, L. G., editor, Martz, G., editor, Mathé, G., editor, Mühlbock, O., editor, Nakahara, W., editor, Potter, V. R., editor, Sabin, A. B., editor, Sachs, L., editor, Saxén, E. A., editor, Spiegelmann, S., editor, Szybalski, W., editor, Tagnon, H., editor, Taylor, R. M., editor, Tissières, A., editor, Uehlinger, E., editor, Wissler, R. W., editor, Yoshida, T., editor, Rentchnick, P., editor, Grundmann, E., editor, and Oettgen, H. F., editor

Published
1970
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14. The T-Cell Receptor/T3 Complex

Author

Terhorst, C., Georgopoulos, K., Gold, P., Oettgen, H., Pettey, C., Ucker, D., van den Elsen, P., Feldmann, Marc, editor, and McMichael, Andrew, editor

Published
1986
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17. Endotoxin-Induced Tumor Necrosis Factor

Author

Oettgen, H. F., Carswell, E. A., Kassel, R. L., Fiore, N., Williamson, B., Hoffmann, M. K., Haranaka, K., Old, L. J., Allfrey, V. G., editor, Allgöwer, M., editor, Berenblum, I., editor, Bergel, F., editor, Bernard, J., editor, Bernhard, W., editor, Blokhin, N. N., editor, Bock, H. E., editor, Braun, W., editor, Bucalossi, P., editor, Chaklin, A. V., editor, Chorazy, M., editor, Cunningham, G. J., editor, Della Porta, G., editor, Denoix, P., editor, Dulbecco, R., editor, Eagle, H., editor, Eker, R., editor, Good, R. A., editor, Grabar, P., editor, Harris, R. J. C., editor, Hecker, E., editor, Herbeuval, R., editor, Higginson, J., editor, Hueper, W. C., editor, Isliker, H., editor, Kieler, J., editor, Kirsten, W. H., editor, Klein, G., editor, Koprowski, H., editor, Koss, L. G., editor, Macbeth, R. A., editor, Martz, G., editor, Mathé, G., editor, Mühlbock, O., editor, Old, L. J., editor, Potter, V. R., editor, Sabin, A. B., editor, Sachs, L., editor, Saxén, E. A., editor, Schmidt, C. G., editor, Spiegelman, S., editor, Szybalski, W., editor, Tagnon, H., editor, Tissières, A., editor, Uehlinger, E., editor, Wissler, R. W., editor, Rentchnick, P., editor, Senn, H. J., editor, Mathé, Georges, editor, and Muggia, Franco M., editor

Published
1980
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18. Tumor-Specific Antigens

Author

Pfreundschuh, M., Shiku, H., Takahashi, T., Ueda, R., Ransohoff, J., Oettgen, H. F., Old, L. J., Allfrey, V. G., editor, Allgöwer, M., editor, Berenblum, I., editor, Bergel, F., editor, Bernard, J., editor, Bernhard, W., editor, Blokhin, N. N., editor, Bock, H. E., editor, Braun, W., editor, Bucalossi, P., editor, Chaklin, A. V., editor, Chorazy, M., editor, Cunningham, G. J., editor, Della Porta, G., editor, Denoix, P., editor, Dulbecco, R., editor, Eagle, H., editor, Eker, R., editor, Good, R. A., editor, Grabar, P., editor, Harris, R. J. C., editor, Hecker, E., editor, Herbeuval, R., editor, Higginson, J., editor, Hueper, W. C., editor, Isliker, H., editor, Kieler, J., editor, Kirsten, W. H., editor, Klein, G., editor, Koprowski, H., editor, Koss, L. G., editor, Macbeth, R. A., editor, Martz, G., editor, Mathé, G., editor, Mühlbock, O., editor, Old, L. J., editor, Potter, V. R., editor, Sabin, A. B., editor, Sachs, L., editor, Saxén, E. A., editor, Schmidt, C. G., editor, Spiegelman, S., editor, Szybalski, W., editor, Tagnon, H., editor, Tissières, A., editor, Uehlinger, E., editor, Wissler, R. W., editor, Rentchnick, P., editor, Senn, H. J., editor, Mathé, Georges, editor, and Muggia, Franco M., editor

Published
1980
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19. Adjuvant Trial of Levamisole in Patients With Squamous Cancer of the Head and Neck: A Preliminary Report

Author

Wanebo, H. J., Hilal, E. Y., Strong, E. W., Pinsky, C. M., Mike, V., Oettgen, H. F., Allfrey, V. G., editor, Allgöwer, M., editor, Berenblum, I., editor, Bergel, F., editor, Bernard, J., editor, Bernhard, W., editor, Blokhin, N. N., editor, Bock, H. E., editor, Braun, W., editor, Bucalossi, P., editor, Chaklin, A. V., editor, Chorazy, M., editor, Cunningham, G. J., editor, Porta, G. Della, editor, Denoix, P., editor, Dulbecco, R., editor, Eagle, H., editor, Eker, R., editor, Good, R. A., editor, Grabar, P., editor, Harris, R. J. C., editor, Hecker, E., editor, Herbeuval, R., editor, Higginson, J., editor, Hueper, W. C., editor, Isliker, H., editor, Kieler, J., editor, Kirsten, W. H., editor, Klein, G., editor, Koprowski, H., editor, Koss, L. G., editor, Martz, G., editor, Mathé, G., editor, Mühlbock, O., editor, Nakahara, W., editor, Old, L. J., editor, Potter, V. R., editor, Sabin, A. B., editor, Sachs, L., editor, Saxén, E. A., editor, Schmidt, C. G., editor, Spiegelman, S., editor, Szybalski, W., editor, Tagnon, H., editor, Taylor, R. M., editor, Tissières, A., editor, Uehlinger, E., editor, Wissler, R. W., editor, Rentchnick, P., editor, Bonadonna, Gianni, editor, Mathé, Georges, editor, and Salmon, Sydney E., editor

Published
1979
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20. Delayed-Hypersensitivity Reactions in Patients with Cancer

Author

Pinsky, C. M., El Domeiri, A., Caron, A. S., Knapper, W. H., Oettgen, H. F., Allfrey, V. G., editor, Allgöwer, M., editor, Bauer, K. H., editor, Berenblum, I., editor, Bergel, F., editor, Bernard, J., editor, Bernhard, W., editor, Blokhin, N. N., editor, Bock, H. E., editor, Bucalossi, P., editor, Chaklin, A. V., editor, Chorazy, M., editor, Cunningham, G. J., editor, Dargent, M., editor, Della Porta, G., editor, Denoix, P., editor, Dulbecco, R., editor, Eagle, H., editor, Eker, E., editor, Good, R. A., editor, Grabar, P., editor, Hamperl, H., editor, Harris, R. J. C., editor, Hecker, E., editor, Herbeuval, R., editor, Higginson, J., editor, Hueper, W. C., editor, Isliker, H., editor, Kieler, J., editor, Klein, G., editor, Koprowski, H., editor, Koss, L. G., editor, Martz, G., editor, Mathé, G., editor, Mühlbock, O., editor, Nakahara, W., editor, Old, L. J., editor, Potter, V. R., editor, Sabin, A. B., editor, Sachs, L., editor, Saxén, E. A., editor, Schmidt, C. G., editor, Spiegelman, S., editor, Szybalski, W., editor, Tagnon, H., editor, Taylor, R. M., editor, Tissières, A., editor, Uehlinger, E., editor, Wissler, R. W., editor, Rentchnick, P., editor, Mathé, Georges, editor, and Weiner, Roy, editor

Published
1974
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28. Monoclonal antibodies and immobilized antibodies

Author

Linhardt, Robert J., Abell C. W., Denney R. M., Altrock B. W., Auerbach R., Bernal S. D., Canfield R. E., Ehrlich P. H., Moyle W. R., Chan T. S., Chang T. W., Chang N. T., Cidlowski J. A., Viceps M. D., Cote R. J., Morrissey D. M., Houghton A. N., Beattie E. J., Oettgen H. F., Old L. J., Croce C. M., Cubicciotti R. S., Karu A. E., Krauss R. M., Cullor J. S., Deutsch A., Brandwein H., Platt H., Hunter D. M., Dubitsky A., Durham S. M., Dolbeare F. A., Gray J. W., Dreesman G. R., Kendall C. E., Egrie J. C., Frackelton A. R., Eisen H. N., Ross A. H., Gay S., Geirnaert G., Geltosky J. E., Goldberg E. H., Goldwasser E., Kavinsky C., Weiss T. L., Gratzner H. G., Hampar B., Zweig M., Showalter S. D., Handley H. H., Glassy M. C., Hagiwara Y., Hagiwara H., Huang C. M., Cohen S. N., Hughes J. V., Scolnick E. M., Tomassini J. E., Jefferis R., Steensgaard J., Kaplan H. S., Teng N. N. H., Earn K. S., Calvo R. F., Kass L., Kettman J. R., Norgard M. V., Khazaeli M. B., Beierwaltes W. H., England B. G., Kung P. C., Goldstein G., Lanier L., Phillips J., Lanier L., Warner N. L., Larrick J. W., Raubitschek A. R., Truitt K. E., Lazarus H., Schwaber J. F., Lewicki J., Lewis C., Olander J. V., Tolbert W. R., Milford E. L., Carpenter C. B., Paradysz J. M., Mosher D. F., Mulshine J. L., Minna J. D., Murray K. A., Neville D. M., Youle R. J., Neville D. M., Youle R. J., Nicolson M., Pastan I., Willingham M. C., Fitzgerald D. J., Pucci A., Smithyman A. M., Slade M. B., French P. W., Wijffels G., Pukel C. S., Lloyd K. O., Travassos L. R., Dippold W. G., Oettgen H. F., Old L. J., Reckel R. P., Harris J. L., Wellerson R., Shaw S. M., Kaplan P. M., Reinherz E. L., Schlossman S. F., Mener S. C., Sakamoto J., Cordon C. C., Friedman E., Finstad C. L., Enker W. E., Melamed M. R., Lloyd K. O., Oettgen J. F., Old L. J., Scannon P. J., Spitler L. E., Lee H. M., Kawahata R. T., Mischak R. P., Schlom J., Colcher D., Nuti M., Hand P. H., Austin F., Shockman G. D., Jackson D. E., Wong W., Steplewski Z., Koprowski H., Herlyn M., Strand M., Trowbridge I. S., Urdal D. L., March C. J., Dower S. K., Wands J. R., Zurawski V. R., White C. A., Dulbecco R., Allen W. R., Arnold E. C., Flasher M., Freedman H. H., Heath T. D., Shek P., Papahadjopoulos D., Ikeda M., Sakamoto S., Suzuki K., Kuboyama M., Harada Y., Kawashiri A., Takahashi E., Lee H. S., Margel S., Neville D. M., Youle R. J., Nowinski R. C., Hoffman A. S., Peterson J. W., Platt K. B., Reed D. E., Real F. X., Mattes M. J., Houghton A. N., Livingston P. O., Lloyd K. O., Oettgen H. F., Old L. J., Rembaum A., Yen R. C. K., Rosenstein R., and Schneider B.

Published
1987
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29. The soluble isoform of human FcɛRI is an endogenous inhibitor of IgE‐mediated mast cell responses.

Author

Moñino‐Romero, S., Erkert, L., Schmidthaler, K., Diesner, S. C., Sallis, B. F., Pennington, L., Jardetzky, T., Oettgen, H. C., Bohle, B., Fiebiger, E., and Szépfalusi, Z.

Subjects
MAST cells, IMMUNOGLOBULIN E, BONE cells, DENDRITIC cells, MEMBRANE proteins, BONES
Abstract

Background: The soluble isoform of FcɛRI, the high‐affinity IgE receptor (sFcεRI), is a protein of the IgE network with poorly defined functions. Objective: To define cellular sources and signals that result in the production of human sFcεRI and study its in vivo functions. Methods: FcεRI‐transfected human cell lines (MelJuso), human monocyte‐derived dendritic cells (moDCs), and murine bone marrow‐derived mast cells (MC) were stimulated by FcεRI cross‐linking and release of sFcεRI was analyzed (ELISA, Western Blot). Lysosomal‐associated membrane protein 1 degranulation assays and human basophil activation tests (BATs) were used to study IgE‐dependent activation. Recombinant sFcεRI (rsFcεRI) was used to assess its role in murine models of anaphylaxis with WT (wild‐type) and IgE−/− (IgE‐deficient) mice. Results: Antigen‐specific cross‐linking of IgE‐loaded FcɛRI on MelJuso cells that express the trimeric or tetrameric receptor isoform induced the production of sFcεRI. Using MCs and moDCs, we confirmed that IgE/FcɛRI activation induces sFcɛRI release. We demonstrated that generation of sFcɛRI requires Src phosphorylation and endo/lysosomal acidification. In experimental mouse models, sFcɛRI diminishes the severity of IgE‐mediated anaphylaxis. BATs confirmed that, comparable to the anti‐IgE monoclonal antibody omalizumab, sFcɛRI is an inhibitor of the human innate IgE effector axis, implying that sFcɛRI and omalizumab potentially inhibit each other in vivo. Conclusion: sFcɛRI is produced after antigen‐specific IgE/FcɛRI‐mediated activation signals and functions as an endogenous inhibitor of IgE loading to FcɛRI and IgE‐mediated activation. Our results imply, therefore, that sFcɛRI contributes to a negative regulatory feedback loop that aims at preventing overshooting responses after IgE‐mediated immune activation. The soluble isoform of FcεRI, sFcεRI is released after antigen‐specific cross‐linking on monocyte‐derived dendritic cells and murine bone marrow‐derived mast cells, where Src phosphorylation and endo/lysosomal acidification are key events. Comparable to omalizumab, sFcεRI prevents IgE binding and activation on human basophils in vitro. In experimental mouse models, sFcεRI diminishes severity of IgE‐mediated anaphylaxis and decreases surface IgE on basophils. [ABSTRACT FROM AUTHOR]

Published
2019
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30. Targeting Lewis Y (LeY) in small cell lung cancer (SCLC) with a humanized monoclonal antibody, hu3S193: A pilot trial testing two dose levels

Author

Krug LM, Milton D, Jungbluth AA, Chen LC, Pandit Taskar N, Nagel A, Jones J, Kris MG, Finn R, Smith Jones P, Oettgen H, Scott AM, Old L, Divgi C., QUAIA, Emilio, Krug, Lm, Milton, D, Jungbluth, Aa, Chen, Lc, Quaia, Emilio, Pandit Taskar, N, Nagel, A, Jones, J, Kris, Mg, Finn, R, Smith Jones, P, Oettgen, H, Scott, Am, Old, L, and Divgi, C.

Subjects
Adult, Male, Pulmonary and Respiratory Medicine, medicine.medical_specialty, Pathology, Lung Neoplasms, Time Factors, medicine.drug_class, medicine.medical_treatment, Bone Neoplasms, Pilot Projects, Antibodies, Monoclonal, Humanized, Monoclonal antibody, Gastroenterology, Immunoglobulin G, lung, Lewis Blood Group Antigens, Monoclonal Antibody Hu3S193, Internal medicine, medicine, Humans, cancer, Tissue Distribution, Carcinoma, Small Cell, Aged, Chemotherapy, biology, Brain Neoplasms, business.industry, Indium Radioisotopes, Liver Neoplasms, Antibodies, Monoclonal, Middle Aged, Radioimmunotherapy, SPECT, Treatment Outcome, Oncology, Monoclonal, biology.protein, Immunohistochemistry, Female, Antibody, business, lung, cancer, SPECT
Abstract

Introduction Lewis Y (Le y ) is a blood group antigen with robust expression on the surface of epithelial tumors, including small cell lung cancer (SCLC), making it a potential target for antibody-based immunotherapy. 3S193, an immunoglobulin G 3 monoclonal antibody, has demonstrated superior specificity, affinity, and cytotoxicity over other anti-Le y antibodies. A phase I trial of humanized 3S193 (hu3S193) with dosing up to 40 mg/m 2 demonstrated tumor targeting without serious toxicities or the development of human anti-human antibodies. Methods We tested the targeting and pharmacokinetics of hu3S193 in patients with SCLC. Eligibility required progressive SCLC treated with up to three previous chemotherapy regimens, measurable disease not previously irradiated, and tumor samples positive for 3S193 by immunohistochemistry. Patients received four weekly injections of hu3S193, five patients at 10 mg/m 2 and five patients at 20 mg/m 2 . The first and fourth injections were radiolabeled with indium-111 for gamma camera imaging. Results Of 40 patients screened, 25 of 34 (74%) assessable SCLC tumor samples were 3S193 positive by immunohistochemistry. Ten patients were treated with hu3S193; nine completed all four injections. All fluorodeoxyglucose (FDG)-avid lesions >2 cm were visualized on antibody single-photon emission computed tomography. Some lesions overlying vascular structures could not be visualized. No difference was noted in imaging or pharmacokinetics between the first and fourth injections. Toxicities included grade 2 urticaria ( n = 1), grade 1 vomiting ( n = 2), and grade 2 hypertension ( n = 1) transiently after infusion at the higher dose. Conclusions Given the strong tumor targeting, particularly at the higher dose, the favorable toxicity profile, and the potential for immunomodulatory effects, hu3S193 warrants further investigation in SCLC.

Published
2007

36. Geschwülste · Tumors I

Author

Alexander, P., primary, Chomette, G., additional, Hamperl, H., additional, Hossfeld, D. K., additional, Koss, L. G., additional, Laumonier, R., additional, Oettgen, H. F., additional, Rajewsky, M. F., additional, Sandberg, A. A., additional, Sobin, L. H., additional, Tulinius, H., additional, and Watanabe, S., additional

Published
1974
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41. Eotaxin triggers eosinophil-selective chemotaxis and calcium flux via a distinct receptor and induces pulmonary eosinophilia in the presence of interleukin 5 in mice

Author

Rothenberg, M. E., Ownbey, R., Mehlhop, P. D., Loiselle, P. M., van de Rijn, M., Bonventre, J. V., Oettgen, H. C., Leder, P., and Luster, A. D.

Subjects
Chemokine CCL11, Lung Diseases, Cell Survival, Chemotactic Factors, Eosinophil, Receptors, CCR3, Mice, Inbred Strains, Mice, Transgenic, Histamine Release, Mice, Eosinophilia, Escherichia coli, Animals, Humans, Cloning, Molecular, Receptors, Cytokine, Cells, Cultured, Macrophages, respiratory system, Recombinant Proteins, Basophils, Eosinophils, Chemotaxis, Leukocyte, Chemokines, CC, Factor Xa, Mice, Inbred CBA, Cytokines, Calcium, Receptors, Chemokine, Interleukin-5, Research Article
Abstract

BACKGROUND: Understanding the processes that control selective eosinophilia is of fundamental importance in a variety of human diseases (e.g., allergies, parasitic infections, malignancy). Interleukin 5, an eosinophil-specific growth and activating factor, and eotaxin appear to collaborate in this process. Eotaxin is a recently described chemotactic factor that belongs to the C-C (or beta) chemokine family and has been implicated in animal and human eosinophilic inflammatory states. We have recently reported the molecular characterization of murine eotaxin and now report the biological properties of purified recombinant murine eotaxin in vitro and in vivo in the presence or absence of interleukin 5 (IL-5) in mice. MATERIALS AND METHODS: Murine eotaxin was expressed in bacteria and purified by affinity chromatography and HPLC. Activity was tested in vitro by examining chemotactic and calcium flux responses of purified murine leukocytes. Additionally, desensitization of calcium flux responses to other chemokines, eosinophil survival assays, and basophil histamine release were examined. Finally, eotaxin was delivered to wild-type or IL-5 transgenic mice and the host response was examined. RESULTS: Eotaxin had activity only when the recombinant molecule had the native mature amino terminus and contained the first 25 amino acids of the mature protein. It was active in vitro at an effective concentration between 10 and 100 ng/ml in both chemotaxis and calcium flux assays toward eosinophils, but not macrophages or neutrophils. Furthermore, intranasal or subcutaneous application of eotaxin selectively recruited large numbers of eosinophils into the mouse lung and skin, respectively, only in the presence of interleukin 5. Macrophage inflammatory protein-1 alpha, a related C-C chemokine active on eosinophils, and eotaxin were not able to cross-desensitize. Eotaxin had no affect on the in vitro survival of eosinophils and did not induce basophil histamine release. CONCLUSIONS: Mouse eotaxin is an eosinophil specific chemoattractant that has a markedly enhanced effect in vivo in the presence of another eosinophil selective cytokine IL-5, and utilizes a signal transduction receptor pathway that is distinct from that utilized by macrophage inflammatory protein-1 alpha. This data suggests that the development of tissue eosinophilia in vivo involves a two-step mechanism elicited by interleukin 5 and eotaxin.

Published
1996

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