Immunosuppressive factors from adult T-cell leukemia cells

The mechanism of immunodeficiency in adult T-cell leukemia (ATL) patients was studied in vitro. Peripheral blood lymphocytes from ATL patients and ATL cell lines such as Hut 102, MT 1, and MT 2 were not activated to proliferate by the stimulation with concanavalin A and suppressed normal lymphocyte...

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Veröffentlicht in:Cancer research (Chicago, Ill.) Ill.), 1986-09, Vol.46 (9), p.4458-4462
Hauptverfasser: SHIRAKAWA, F, TANAKA, Y, ODA, S, CHIBA, S, SUZUKI, H, ETO, S, YAMASHITA, U
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container_end_page 4462
container_issue 9
container_start_page 4458
container_title Cancer research (Chicago, Ill.)
container_volume 46
creator SHIRAKAWA, F
TANAKA, Y
ODA, S
CHIBA, S
SUZUKI, H
ETO, S
YAMASHITA, U
description The mechanism of immunodeficiency in adult T-cell leukemia (ATL) patients was studied in vitro. Peripheral blood lymphocytes from ATL patients and ATL cell lines such as Hut 102, MT 1, and MT 2 were not activated to proliferate by the stimulation with concanavalin A and suppressed normal lymphocyte proliferative responses induced with concanavalin A when cultured together. The sera from ATL patients and the culture supernatants from ATL cells and ATL cell lines also suppressed normal lymphocyte proliferative responses induced with concanavalin A. By Sephacryl S-200 column chromatography, the suppressive factors were fractionated as a single peak with the molecular weights of 50,000 to 70,000. The suppressive factors were unstable to acid treatment but stable to the treatment with base, heat, freezing-thawing, and trypsin. The factors suppressed the production of interleukin 2 by T-cells and the responsiveness of T-cells to interleukin 2, but not the expression of interleukin 2 receptors on T-cells and the production of interleukin 1 by monocytes. These results suggest that the immunosuppressive factors produced by ATL cells have some roles in the induction of immunodeficient states in ATL patients.
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Peripheral blood lymphocytes from ATL patients and ATL cell lines such as Hut 102, MT 1, and MT 2 were not activated to proliferate by the stimulation with concanavalin A and suppressed normal lymphocyte proliferative responses induced with concanavalin A when cultured together. The sera from ATL patients and the culture supernatants from ATL cells and ATL cell lines also suppressed normal lymphocyte proliferative responses induced with concanavalin A. By Sephacryl S-200 column chromatography, the suppressive factors were fractionated as a single peak with the molecular weights of 50,000 to 70,000. The suppressive factors were unstable to acid treatment but stable to the treatment with base, heat, freezing-thawing, and trypsin. The factors suppressed the production of interleukin 2 by T-cells and the responsiveness of T-cells to interleukin 2, but not the expression of interleukin 2 receptors on T-cells and the production of interleukin 1 by monocytes. 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Peripheral blood lymphocytes from ATL patients and ATL cell lines such as Hut 102, MT 1, and MT 2 were not activated to proliferate by the stimulation with concanavalin A and suppressed normal lymphocyte proliferative responses induced with concanavalin A when cultured together. The sera from ATL patients and the culture supernatants from ATL cells and ATL cell lines also suppressed normal lymphocyte proliferative responses induced with concanavalin A. By Sephacryl S-200 column chromatography, the suppressive factors were fractionated as a single peak with the molecular weights of 50,000 to 70,000. The suppressive factors were unstable to acid treatment but stable to the treatment with base, heat, freezing-thawing, and trypsin. The factors suppressed the production of interleukin 2 by T-cells and the responsiveness of T-cells to interleukin 2, but not the expression of interleukin 2 receptors on T-cells and the production of interleukin 1 by monocytes. 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Malignant lymphomas. Malignant reticulosis. Myelofibrosis</topic><topic>Lymphocyte Activation</topic><topic>Medical sciences</topic><topic>Monocytes - immunology</topic><topic>Receptors, Immunologic - metabolism</topic><topic>Receptors, Interleukin-2</topic><topic>T-Lymphocytes - immunology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>SHIRAKAWA, F</creatorcontrib><creatorcontrib>TANAKA, Y</creatorcontrib><creatorcontrib>ODA, S</creatorcontrib><creatorcontrib>CHIBA, S</creatorcontrib><creatorcontrib>SUZUKI, H</creatorcontrib><creatorcontrib>ETO, S</creatorcontrib><creatorcontrib>YAMASHITA, U</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>MEDLINE - Academic</collection><jtitle>Cancer research (Chicago, Ill.)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>SHIRAKAWA, F</au><au>TANAKA, Y</au><au>ODA, S</au><au>CHIBA, S</au><au>SUZUKI, H</au><au>ETO, S</au><au>YAMASHITA, U</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Immunosuppressive factors from adult T-cell leukemia cells</atitle><jtitle>Cancer research (Chicago, Ill.)</jtitle><addtitle>Cancer Res</addtitle><date>1986-09-01</date><risdate>1986</risdate><volume>46</volume><issue>9</issue><spage>4458</spage><epage>4462</epage><pages>4458-4462</pages><issn>0008-5472</issn><eissn>1538-7445</eissn><coden>CNREA8</coden><abstract>The mechanism of immunodeficiency in adult T-cell leukemia (ATL) patients was studied in vitro. Peripheral blood lymphocytes from ATL patients and ATL cell lines such as Hut 102, MT 1, and MT 2 were not activated to proliferate by the stimulation with concanavalin A and suppressed normal lymphocyte proliferative responses induced with concanavalin A when cultured together. The sera from ATL patients and the culture supernatants from ATL cells and ATL cell lines also suppressed normal lymphocyte proliferative responses induced with concanavalin A. By Sephacryl S-200 column chromatography, the suppressive factors were fractionated as a single peak with the molecular weights of 50,000 to 70,000. The suppressive factors were unstable to acid treatment but stable to the treatment with base, heat, freezing-thawing, and trypsin. The factors suppressed the production of interleukin 2 by T-cells and the responsiveness of T-cells to interleukin 2, but not the expression of interleukin 2 receptors on T-cells and the production of interleukin 1 by monocytes. These results suggest that the immunosuppressive factors produced by ATL cells have some roles in the induction of immunodeficient states in ATL patients.</abstract><cop>Philadelphia, PA</cop><pub>American Association for Cancer Research</pub><pmid>2873886</pmid><tpages>5</tpages></addata></record>
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source MEDLINE; American Association for Cancer Research; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals
subjects AIDS/HIV
Biological and medical sciences
Cell Line
Concanavalin A - pharmacology
Deltaretrovirus Infections - immunology
Hematologic and hematopoietic diseases
Histocompatibility Antigens Class II - immunology
HLA-DR Antigens
Humans
Immune Tolerance
Immunosuppressive Agents - analysis
Immunosuppressive Agents - immunology
Interleukin-1 - biosynthesis
Interleukin-2 - biosynthesis
Leukemias. Malignant lymphomas. Malignant reticulosis. Myelofibrosis
Lymphocyte Activation
Medical sciences
Monocytes - immunology
Receptors, Immunologic - metabolism
Receptors, Interleukin-2
T-Lymphocytes - immunology
title Immunosuppressive factors from adult T-cell leukemia cells
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