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      Transforming Growth Factor-β 1 Inhibits Vascular Permeability Factor Release by T Cells in Normal Subjects and in Patients with Minimal-Change Nephrotic Syndrome

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          Abstract

          Background/Aim: A lymphokine, the vascular permeability factor (VPF), which increases vascular permeability, has been characterized in minimal-change nephrotic syndrome (MCNS). Transforming growth factor-β (TGF-β) is an immunosuppressive cytokine that inhibits proliferation, cytokine production, and cytotoxic activity of T cells and natural killer cells. We, therefore, investigated the effects of TGF-β<sub>1</sub> on the release of VPF by peripheral blood T cells from MCNS patients. The aim of our study was to determine the in vitro immunosuppressive capacity of TGF-β<sub>1</sub> in patients with MCNS. Methods: To further test the effect of TGF-β<sub>1</sub> on concanavalin A (Con A)-induced VPF release, normal and MCNS T cells were stimulated with 5 µg/ml of Con A in the presence or absence of TGF-β<sub>1</sub>, and the culture supernatants were tested for the presence of VPF by the method of Lagrue et al. The disease controls included 16 patients with IgA nephropathy. Results: Significantly increased spontaneous and Con A-stimulated secretion of VPF was detected in T-cell cultures of MCNS patients with the nephrotic syndrome as compared with those of normal controls. Addition of TGF-β<sub>1</sub> to these cultures inhibited the release of VPF in a dose-dependent manner. The effect of TGF-β<sub>1</sub> on the release of VPF was specific, since a reversion was obtained with a neutralizing monoclonal antibody to human TGF-β<sub>1</sub>. Conclusion: Together, our data demonstrate that TGF-β<sub>1</sub> antagonizes the ability of T cells to release VPF, and suggest a role of TGF-β<sub>1</sub> in the pathophysiology of VPF in vitro.

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          Inflammatory and immunomodulatory roles of TGF-β

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            Interleukin-4 Cooperates with Interleukin-10 to Inhibit Vascular Permeability Factor Release by Peripheral Blood Mononuclear Cells from Patients with Minimal-Change Nephrotic Syndrome

            Increased production of a vascular permeability factor (VPF) from peripheral blood mononuclear cells (PBMC) in patients with minimal-change nephrotic syndrome (MCNS) has been reported. Interleukin-4 (IL-4) and interleukin-10 (IL-10), both produced by T-helper type-2 cells, are cytokines with the capacity to downregulate proinflammatory responses. To gain insight into the immunoregulatory properties of these cytokines, we analyzed the effects of recombinant human IL-4 and IL-10 on VPF release in MCNS patients. In the present study we show that the regulatory cytokines IL-4 and IL-10 are potent inhibitors of the VPF activity of concanavalin A-activated MCNS PBMC. Each cytokine was found to suppress VPF release in a dose-dependent manner. Moreover, when used at suboptimal concentrations, a combination of the two cytokines resulted in enhanced suppression of VPF release. Neutralization of endogenously produced IL-4 and IL-10 by both anti-IL-4 and anti-IL-10 antibodies resulted in an increased release of VPF. These data demonstrate that IL-4 acts in concert with IL-10 to inhibit VPF release and suggest that they are effective biologic regulators of the VPF responses in vitro.
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              Author and article information

              Journal
              NEF
              Nephron
              10.1159/issn.1660-8151
              Nephron
              S. Karger AG
              1660-8151
              2235-3186
              2001
              2001
              16 February 2001
              : 87
              : 2
              : 111-117
              Affiliations
              aDepartment of Medical Technology, College of Medical Sciences, Saitama Prefectural University, Koshigaya, Saitama, and bSecond Department of Internal Medicine, Nihon University School of Medicine, Tokyo, Japan
              Article
              45898 Nephron 2001;87:111–117
              10.1159/000045898
              11244304
              © 2001 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: 3, References: 24, Pages: 7
              Product
              Self URI (application/pdf): https://www.karger.com/Article/Pdf/45898
              Categories
              Original Paper

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