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      Substance-P-Mediated Immunomodulation of Tumor Growth in a Murine Model

      ,

      Neuroimmunomodulation

      S. Karger AG

      Neuroimmunomodulation, Neuropeptide, Tumor growth, Substance P

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          Abstract

          Background/Objective: Substance P (SP) has been reported to have immunoregulatory properties including effects on many of the mediators involved in anti-tumor immunity. In this study, we investigated the effect of SP on tumor development in a murine model of melanoma. In addition, we examined the role of natural killer (NK) and T cells in SP-mediated modulation of tumor growth. Materials and Methods: Mice were implanted with mini-osmotic pumps that delivered a continuous infusion of either SP or PBS over a 14-day period. Five days following implantation, animals received K1735 melanoma cells and tumor growth was monitored. The role of NK and T cells in SP-mediated protection was examined by antibody depletion studies. To determine if cells from SP-treated animals could delay tumor growth in animals in the absence of exogenous SP infusion, splenocytes from mice treated with SP were adoptively transferred into SCID mice. Results: In vivoSP treatment led to a significant delay in tumor growth. When animals were depleted of NK or T cells, this protective effect was lost. Adoptive transfer of cells from SP-treated animals led to a significant protective effect on tumor growth in SCID mice. Conclusion: Pretreatment of mice with SP provides protection against K1735 tumor growth, and this protection requires both T cells and NK cells. SP-mediated tumor protection can be transferred by the adoptive transfer of cells from SP-treated animals into animals that do not receive exogenous SP. These studies suggest a model in which in vivo SP treatment prior to tumor challenge primes immune mediators to prevent or delay tumor establishment.

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          Most cited references 37

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          Response of resting human peripheral blood natural killer cells to interleukin 2

          The present study shows that recombinant interleukin 2 (IL-2) purified to homogeneity induces a rapid and potent enhancement of spontaneous cytotoxicity of human peripheral blood lymphocytes. The cells mediating cytotoxicity after 18-h treatment with IL-2 have surface markers of natural killer (NK) cells and are generated from the peripheral blood subset containing spontaneous cytotoxic cells. A parallel production of gamma interferon (IFN-gamma) is induced by recombinant IL-2 (rIL-2), and NK cells appear to be the major producer cells, whereas T cells are unable to produce IFN-gamma under these experimental conditions. However, the kinetics of the enhancement of cytotoxicity are faster than those of IFN-gamma production, and monoclonal anti-IFN-gamma antibodies do not suppress this effect, making it unlikely that the IFN- gamma produced is responsible for the enhancement. The enhancement of NK cell activity induced by rIL-2 precedes any proliferative response of the lymphocytes, which is instead observed in longer-term cultures of both NK and T cells.
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            Interleukin-2 augments natural killer cell activity.

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              ‘Nude’, a new hairless gene with pleiotropic effects in the mouse

               S Flanagan (1966)
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                Author and article information

                Journal
                NIM
                Neuroimmunomodulation
                10.1159/issn.1021-7401
                Neuroimmunomodulation
                S. Karger AG
                1021-7401
                1423-0216
                2005
                June 2005
                27 June 2005
                : 12
                : 4
                : 201-210
                Affiliations
                Department of Biology, University of St. Thomas, St. Paul, Minn., USA
                Article
                85652 Neuroimmunomodulation 2005;12:201–210
                10.1159/000085652
                15990451
                © 2005 S. Karger AG, Basel

                Copyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher. Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug. Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements.

                Page count
                Figures: 6, References: 72, Pages: 10
                Categories
                Original Paper

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