Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
1991-2-19
pubmed:abstractText
Using a dimethylbenzanthracene-induced immunogenic nonmetastatic murine mammary adenocarcinoma in BALB/c mice, our previous work has shown that splenocytes from tumor bearers have reduced responses to both mitogens and Ag including tumor-associated Ag. NK and cytotoxic T cell activities are also reduced in splenocytes of tumor bearers. Mac-1+2+ macrophages induced in mammary tumor bearers are capable of down-regulating lymphocyte responses to mitogens and tumor-associated Ag by cell to cell contact interaction and increased PGE2 production. We have found that the tumor constitutively releases a granulocyte-macrophage (GM)-CSF-like factor in vivo and in vitro, which may be responsible for the systemic increase in cells of the macrophage lineage in tumor-bearing mice. A tumor cell line established from the in vivo tumor expresses and releases GM-CSF as shown by Northern and Western blot analyses. Daily i.p. injections for 3 wk of 10,000 U of rGM-CSF into normal mice induces hemopoietic and immunologic alterations similar to those observed in tumor bearers. Mac-1+ and/or Mac-2+ macrophages can also be detected in the spleens and bone marrow of the mice treated with rGM-CSF. Additionally, splenocytes from rGM-CSF-treated mice have reduced responses to mitogens and their peritoneal exudate cells can cause in vitro down-regulation of proliferative responses of lymphocytes from normal mice. The suppression can be partially reversed by the addition of indomethacin to the cultures suggesting that PGE2 may contribute to the effect. rGM-CSF enhances the in vitro release of PGE2 by the spleen, bone marrow, and peritoneal cells of normal mice. These data indicate that the high levels of GM-CSF constitutively produced by the tumor may be responsible for the hemopoietic changes and immunologic alterations observed in tumor-bearing mice.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
0022-1767
pubmed:author
pubmed:issnType
Print
pubmed:day
15
pubmed:volume
146
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
783-9
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed-meshheading:1824777-Adenocarcinoma, pubmed-meshheading:1824777-Adjuvants, Immunologic, pubmed-meshheading:1824777-Animals, pubmed-meshheading:1824777-Antigens, Differentiation, pubmed-meshheading:1824777-Bone Marrow Cells, pubmed-meshheading:1824777-Dinoprostone, pubmed-meshheading:1824777-Down-Regulation, pubmed-meshheading:1824777-Female, pubmed-meshheading:1824777-Galectin 3, pubmed-meshheading:1824777-Granulocyte-Macrophage Colony-Stimulating Factor, pubmed-meshheading:1824777-Indomethacin, pubmed-meshheading:1824777-Macrophage-1 Antigen, pubmed-meshheading:1824777-Macrophages, pubmed-meshheading:1824777-Male, pubmed-meshheading:1824777-Mammary Neoplasms, Experimental, pubmed-meshheading:1824777-Mice, pubmed-meshheading:1824777-Mice, Inbred BALB C, pubmed-meshheading:1824777-Mitogens, pubmed-meshheading:1824777-Recombinant Proteins, pubmed-meshheading:1824777-Spleen, pubmed-meshheading:1824777-T-Lymphocytes, Regulatory
pubmed:year
1991
pubmed:articleTitle
The role of tumor-derived cytokines on the immune system of mice bearing a mammary adenocarcinoma. I. Induction of regulatory macrophages in normal mice by the in vivo administration of rGM-CSF.
pubmed:affiliation
Department of Microbiology and Immunology (R-138), University of Miami School of Medicine, FL 33101.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.