Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
1998-9-28
pubmed:abstractText
Although macrophages (Mphis) mediate tumor cytotoxicity, display tumor-associated antigens, and stimulate antitumor lymphocytes, cancer cells routinely circumvent these host-mediated immune activities, rendering the host incapable of mounting a successful antitumor immune response. Evidence supporting a direct causal relationship between cancer and immune dysfunction suggests that the presence of neoplastic tissue leads to immunologic degeneration. Furthermore, substantial data demonstrate that tumor growth adversely alters Mphi function and phenotype. Thus, although Mphis can serve as both positive and negative mediators of the immune system, the importance of Mphis in tumor-induced immune suppression remains controversial. This review focuses on the evidence that tumor-derived molecules redirect Mphi activities to promote tumor development. Tumors produce cytokines, growth factors, chemotactic molecules, and proteases that influence Mphi functions. Many tumor-derived molecules, such as IL-4, IL-6, IL-10, MDF, TGF-beta1, PGE2, and M-CSF, deactivate or suppress the cytotoxic activity of activated Mphis. Evidence that tumor-derived molecules modulate Mphi cytotoxicity and induce Mphi suppressor activity is presented. This information further suggests that Mphis in different in vivo compartments may be differentially regulated by tumor-derived molecules, which may deactivate tumor-proximal (in situ) Mphi populations while concurrently activating tumor-distal Mphis, imparting a twofold insult to the host's antitumor immune response.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
0741-5400
pubmed:author
pubmed:issnType
Print
pubmed:volume
64
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
275-90
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1998
pubmed:articleTitle
Tumor-induced immune dysfunction: the macrophage connection.
pubmed:affiliation
Department of Biology, Virginia Polytechnic Institute and State University, Blacksburg 24061-0406, USA. kdelgert@vt.edu
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Review, Research Support, Non-U.S. Gov't