| Activation of the IL-1 pathway during amplification of immune responses in tumor-bearing mice. | |
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MedLine Citation:
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PMID: 3493084 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Previous work identified certain components of the immunological network that had been activated following the adoptive immunotherapy of tumor-bearing mice. The present report shows that part of the activation process involves the IL-1 pathway. Tumor-associated macrophages (TAM) from C57BL/6J mice bearing the immunogenic sarcoma, MCA/76-9, and tumor-bearers injected with cyclophosphamide (CY) or CY plus the intravenous transfer of tumor-sensitized lymphocytes showed relatively high levels of intracellular (IC) IL-1, as demonstrated in the mitogenic and comitogenic assays. Gel chromatography of IC IL-1 and extracellular (EC) IL-1 from TAM induced to secrete IL-1 by stimulation with lipopolysaccharide indicated a single peak of activity of similar molecular size. The active fractions of the EC IL-1 were found to increase in activity as they were diluted to a maximum of 1/64, beyond which IL-1 activity declined. Fractions of the IC IL-1 showed no increased activity on dilution. Filtrates (less than 10 kDa) obtained on concentration of the IC and EC IL-1 samples prior to fractionation were shown to contain an activity (3-5 kDa) that inhibited the uptake of [3H]TdR by thymocytes in the mitogenic and comitogenic assays. Membrane-bound IL-1 activity also was expressed by TAM and this coincided with the previously reported peak Ia expression by these cells. TAM were also shown to induce strong proliferative responses by allogeneic lymphocyte. Systemic amplification of antitumor responses was detected in mice bearing progressing tumors and in those that had received combination therapy as measured both by increases in free IL-1 in the peritoneal cavity and IL-1 within the peritoneal macrophages. These observations indicate that in addition to enhancement of Ia expression, the IL-1 pathway also is activated and amplified systemically in this model system of tumor progression and rejection. |
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Authors:
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R Evans; T M Duffy |
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Publication Detail:
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Type: Comparative Study; Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S. |
Journal Detail:
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Title: Cellular immunology Volume: 105 ISSN: 0008-8749 ISO Abbreviation: Cell. Immunol. Publication Date: 1987 Mar |
Date Detail:
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Created Date: 1987-04-23 Completed Date: 1987-04-23 Revised Date: 2007-11-14 |
Medline Journal Info:
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Nlm Unique ID: 1246405 Medline TA: Cell Immunol Country: UNITED STATES |
Other Details:
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Languages: eng Pagination: 86-98 Citation Subset: IM |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Animals Antibody Formation Antigens, Neoplasm / immunology* Histocompatibility Antigens Class II / immunology Immunization, Passive Interleukin-1 / metabolism* Macrophages / immunology Mice Mice, Inbred Strains Sarcoma, Experimental / immunology, pathology |
| Grant Support | |
ID/Acronym/Agency:
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CA 27523/CA/NCI NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Antigens, Neoplasm; 0/Histocompatibility Antigens Class II; 0/Interleukin-1 |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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