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PredicateObject
rdf:type
lifeskim:mentions
pubmed:dateCreated
2002-6-27
pubmed:abstractText
An efficient immune response comprises a highly intricate, integrated circuitry involving both the cellular and the humoral arms of the immune system of the host interacting with the rapidly proliferating microcosm of the tumor The mechanism of tumor rejection involving multiple arms of the immune system was reviewed in a spontaneously regressing rat histiocytoma, AK-5, an autologous tumor-host system. Intraperitoneal tumor transplantation leads to death in all animals, whereas subcutaneously (s.c.) transplanted tumor undergoes regression in 70% of animals. Regression of the tumor occurs by both apoptosis and necrosis, and natural killer (NK) cells were identified as the chief effectors mediating tumor cell death in vivo. A type 1 helper T cell (Th1)-driven cytokine cascade played a crucial role in enhancing cellular functions at the tumor site and obtaining a sufficient immune response for tumor rejection. The s.c. tumor-bearing hosts were shown to produce a factor which induced apoptosis in tumor cells, mediating tumor rejection. This review emphasizes the daunting complexities and interesting liaisons between the host immune system and the tumor, highlighting the work from our laboratory, and stressing that it is the interaction of several factors in concert or antagonizing each other that is responsible for the spontaneous regression of a tumor.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
0105-2896
pubmed:author
pubmed:issnType
Print
pubmed:volume
184
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
244-57
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
2001
pubmed:articleTitle
Host-tumor interactions during the regression of a rat histiocytoma, AK-5.
pubmed:affiliation
Centre for Cellular & Molecular Biology, Hyderabad, India. khar@ccmb.ap.nic.in
pubmed:publicationType
Journal Article, Review, Research Support, Non-U.S. Gov't