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Production of the second component of complement by human monocytes: stimulation by antigen-activated lymphocytes or lymphokines

Human peripheral blood mononuclear cells cultured in the presence of antigen produced hemolytically active second complement component earlier and in larger amounts than did control cultures of the same cells without antigen. The increased amount of C2 in culture supernates came primarily from the a...

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Formato: Texto
Lenguaje:English
Publicado: The Rockefeller University Press 1977
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Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2180649/
https://www.ncbi.nlm.nih.gov/pubmed/858999
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collection PubMed
description Human peripheral blood mononuclear cells cultured in the presence of antigen produced hemolytically active second complement component earlier and in larger amounts than did control cultures of the same cells without antigen. The increased amount of C2 in culture supernates came primarily from the adherent cell population and was due to increased synthesis as demonstrated by inhibition with 10(-4) M cycloheximide. Purified adherent monocytes produced more C2 when exposed to lymphokine-rich supernates from antigen-stimulated lymphocytes than when exposed to control supernates from unstimulated lymphocyte cultures. The increased synthesis of C2, which appeared to be mediated by a lymphokine, was partially inhibited specifically by 0.025 M alpha-L(-) fucose, a sugar which has previously been shown in inhibit the response of macrophages to migration inhibitory factor.
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spelling pubmed-21806492008-04-17 Production of the second component of complement by human monocytes: stimulation by antigen-activated lymphocytes or lymphokines J Exp Med Articles Human peripheral blood mononuclear cells cultured in the presence of antigen produced hemolytically active second complement component earlier and in larger amounts than did control cultures of the same cells without antigen. The increased amount of C2 in culture supernates came primarily from the adherent cell population and was due to increased synthesis as demonstrated by inhibition with 10(-4) M cycloheximide. Purified adherent monocytes produced more C2 when exposed to lymphokine-rich supernates from antigen-stimulated lymphocytes than when exposed to control supernates from unstimulated lymphocyte cultures. The increased synthesis of C2, which appeared to be mediated by a lymphokine, was partially inhibited specifically by 0.025 M alpha-L(-) fucose, a sugar which has previously been shown in inhibit the response of macrophages to migration inhibitory factor. The Rockefeller University Press 1977-05-01 /pmc/articles/PMC2180649/ /pubmed/858999 Text en This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.rupress.org/terms). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 4.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/4.0/).
spellingShingle Articles
Production of the second component of complement by human monocytes: stimulation by antigen-activated lymphocytes or lymphokines
title Production of the second component of complement by human monocytes: stimulation by antigen-activated lymphocytes or lymphokines
title_full Production of the second component of complement by human monocytes: stimulation by antigen-activated lymphocytes or lymphokines
title_fullStr Production of the second component of complement by human monocytes: stimulation by antigen-activated lymphocytes or lymphokines
title_full_unstemmed Production of the second component of complement by human monocytes: stimulation by antigen-activated lymphocytes or lymphokines
title_short Production of the second component of complement by human monocytes: stimulation by antigen-activated lymphocytes or lymphokines
title_sort production of the second component of complement by human monocytes: stimulation by antigen-activated lymphocytes or lymphokines
topic Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2180649/
https://www.ncbi.nlm.nih.gov/pubmed/858999