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Selection of HTLV-I positive clones is prevented by prostaglandin A in infected cord blood cultures.

Type A prostaglandins (PGA1 and 16,16-dimethyl-PGA2-methyl ester) were found to block the proliferation of HTLV-I infected cord blood lymphocytes (CBL) in vitro, thus preventing the clonal immortalisation that is considered as a predisposing condition to HTLV-I positive leukaemia. PGA1 and di-M-PGA2...

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Autores principales: D'Onofrio, C., Alvino, E., Garaci, E., Bonmassar, E., Santoro, M. G.
Formato: Texto
Lenguaje:English
Publicado: Nature Publishing Group 1990
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1971418/
https://www.ncbi.nlm.nih.gov/pubmed/2310673
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author D'Onofrio, C.
Alvino, E.
Garaci, E.
Bonmassar, E.
Santoro, M. G.
author_facet D'Onofrio, C.
Alvino, E.
Garaci, E.
Bonmassar, E.
Santoro, M. G.
author_sort D'Onofrio, C.
collection PubMed
description Type A prostaglandins (PGA1 and 16,16-dimethyl-PGA2-methyl ester) were found to block the proliferation of HTLV-I infected cord blood lymphocytes (CBL) in vitro, thus preventing the clonal immortalisation that is considered as a predisposing condition to HTLV-I positive leukaemia. PGA1 and di-M-PGA2 did not affect the long-term survival of normal non-infected CBL, whereas they suppressed the proliferation of an established cord-blood derived HTLV-I positive cell line, MT-2. As shown by the number of HTLV-I infected p19+ cells, the block of the selection of immortalised, infected clones by PGAs did not appear to be due to an inhibition of early stages of HTLV-I infection. The possibility that the effect of PGAs could be mediated by an action on the immune response was also examined. PGAs regulated the cell-mediated cytotoxic function of CBL to a different extent when normal non-infected or HTLV-I exposed CBL were compared. In fact, PGAs down-regulated the natural killing and macrophage/lymphocyte cytotoxic response of normal CBL, whereas they did not modify the already depressed immune response of CBL challenged with HTLV-I. These results suggest that the protective effect of PGAs against HTLV-I infection in vitro is mostly related to the direct suppression of the clonal expansion of virus-infected cells, rather than to the anti-viral activity or modulation of the cell-mediated immunity. IMAGES:
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spelling pubmed-19714182009-09-10 Selection of HTLV-I positive clones is prevented by prostaglandin A in infected cord blood cultures. D'Onofrio, C. Alvino, E. Garaci, E. Bonmassar, E. Santoro, M. G. Br J Cancer Research Article Type A prostaglandins (PGA1 and 16,16-dimethyl-PGA2-methyl ester) were found to block the proliferation of HTLV-I infected cord blood lymphocytes (CBL) in vitro, thus preventing the clonal immortalisation that is considered as a predisposing condition to HTLV-I positive leukaemia. PGA1 and di-M-PGA2 did not affect the long-term survival of normal non-infected CBL, whereas they suppressed the proliferation of an established cord-blood derived HTLV-I positive cell line, MT-2. As shown by the number of HTLV-I infected p19+ cells, the block of the selection of immortalised, infected clones by PGAs did not appear to be due to an inhibition of early stages of HTLV-I infection. The possibility that the effect of PGAs could be mediated by an action on the immune response was also examined. PGAs regulated the cell-mediated cytotoxic function of CBL to a different extent when normal non-infected or HTLV-I exposed CBL were compared. In fact, PGAs down-regulated the natural killing and macrophage/lymphocyte cytotoxic response of normal CBL, whereas they did not modify the already depressed immune response of CBL challenged with HTLV-I. These results suggest that the protective effect of PGAs against HTLV-I infection in vitro is mostly related to the direct suppression of the clonal expansion of virus-infected cells, rather than to the anti-viral activity or modulation of the cell-mediated immunity. IMAGES: Nature Publishing Group 1990-02 /pmc/articles/PMC1971418/ /pubmed/2310673 Text en https://creativecommons.org/licenses/by/4.0/This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit https://creativecommons.org/licenses/by/4.0/.
spellingShingle Research Article
D'Onofrio, C.
Alvino, E.
Garaci, E.
Bonmassar, E.
Santoro, M. G.
Selection of HTLV-I positive clones is prevented by prostaglandin A in infected cord blood cultures.
title Selection of HTLV-I positive clones is prevented by prostaglandin A in infected cord blood cultures.
title_full Selection of HTLV-I positive clones is prevented by prostaglandin A in infected cord blood cultures.
title_fullStr Selection of HTLV-I positive clones is prevented by prostaglandin A in infected cord blood cultures.
title_full_unstemmed Selection of HTLV-I positive clones is prevented by prostaglandin A in infected cord blood cultures.
title_short Selection of HTLV-I positive clones is prevented by prostaglandin A in infected cord blood cultures.
title_sort selection of htlv-i positive clones is prevented by prostaglandin a in infected cord blood cultures.
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1971418/
https://www.ncbi.nlm.nih.gov/pubmed/2310673
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