Cargando…
IP-10, a -C-X-C- chemokine, elicits a potent thymus-dependent antitumor response in vivo
IP-10 is a member of the -C-X-C-chemokine superfamily of proinflammatory cytokines whose secretion is induced by interferon gamma (IFN-gamma) and lipopolysaccharide (LPS). To date no function has been described for IP-10. We have genetically engineered tumor cells to secrete high levels of murine IP...
Formato: | Texto |
---|---|
Lenguaje: | English |
Publicado: |
The Rockefeller University Press
1993
|
Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2191174/ https://www.ncbi.nlm.nih.gov/pubmed/8350046 |
_version_ | 1782146942807048192 |
---|---|
collection | PubMed |
description | IP-10 is a member of the -C-X-C-chemokine superfamily of proinflammatory cytokines whose secretion is induced by interferon gamma (IFN-gamma) and lipopolysaccharide (LPS). To date no function has been described for IP-10. We have genetically engineered tumor cells to secrete high levels of murine IP-10 and demonstrate that while IP-10 has no effect on the growth of these tumor cells in culture, it elicits a powerful host-mediated antitumor effect in vivo. The IP-10 antitumor response is T lymphocyte dependent, non-cell autonomous, and appears to be mediated by the recruitment of an inflammatory infiltrate composed of lymphocytes, neutrophils, and monocytes. These results document an important biologic property of IP-10 and raise the possibility that some of the T cell-directed effects of IFN-gamma and LPS may be mediated by this chemokine. |
format | Text |
id | pubmed-2191174 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 1993 |
publisher | The Rockefeller University Press |
record_format | MEDLINE/PubMed |
spelling | pubmed-21911742008-04-16 IP-10, a -C-X-C- chemokine, elicits a potent thymus-dependent antitumor response in vivo J Exp Med Articles IP-10 is a member of the -C-X-C-chemokine superfamily of proinflammatory cytokines whose secretion is induced by interferon gamma (IFN-gamma) and lipopolysaccharide (LPS). To date no function has been described for IP-10. We have genetically engineered tumor cells to secrete high levels of murine IP-10 and demonstrate that while IP-10 has no effect on the growth of these tumor cells in culture, it elicits a powerful host-mediated antitumor effect in vivo. The IP-10 antitumor response is T lymphocyte dependent, non-cell autonomous, and appears to be mediated by the recruitment of an inflammatory infiltrate composed of lymphocytes, neutrophils, and monocytes. These results document an important biologic property of IP-10 and raise the possibility that some of the T cell-directed effects of IFN-gamma and LPS may be mediated by this chemokine. The Rockefeller University Press 1993-09-01 /pmc/articles/PMC2191174/ /pubmed/8350046 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 IP-10, a -C-X-C- chemokine, elicits a potent thymus-dependent antitumor response in vivo |
title | IP-10, a -C-X-C- chemokine, elicits a potent thymus-dependent antitumor response in vivo |
title_full | IP-10, a -C-X-C- chemokine, elicits a potent thymus-dependent antitumor response in vivo |
title_fullStr | IP-10, a -C-X-C- chemokine, elicits a potent thymus-dependent antitumor response in vivo |
title_full_unstemmed | IP-10, a -C-X-C- chemokine, elicits a potent thymus-dependent antitumor response in vivo |
title_short | IP-10, a -C-X-C- chemokine, elicits a potent thymus-dependent antitumor response in vivo |
title_sort | ip-10, a -c-x-c- chemokine, elicits a potent thymus-dependent antitumor response in vivo |
topic | Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2191174/ https://www.ncbi.nlm.nih.gov/pubmed/8350046 |