Linked Life Data

3029234

Source:http://linkedlifedata.com/resource/pubmed/id/3029234

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2-3
pubmed:dateCreated
1987-4-13
pubmed:abstractText
Neonatal infection of C57BL/10 mice with cloned ecotropic and/or dualtropic mink cell focus-inducing (MCF) mouse leukaemia viruses (MuLV), induces a wide spectrum of different lymphomas of T, B, and non-T/non-B cell types. The H-2 complex has a marked influence on both the development of lymphoma incidence and lymphoma type. A study using the oncogenic MCF 1233 virus and a series of B10 congenic mice enabled the mapping of the following: Resistance to the early development of T cell lymphoma is controlled by the H-2I-A locus. Susceptibility to early T cell lymphomagenesis is associated with an I-A-regulated low anti-MCF 1233 envelope antibody response and persistent infection of the thymus. B10 (H-2b) mice, which are resistant to early T cell lymphomagenesis induced by MCF 1233 or other MuLV isolates, have high anti-MuLV envelope antibody responses which are I-A-regulated. These mice develop more B cell lymphomas late in life in contrast to the early development of T cell lymphoma in B10.A (H-2a) mice. The possible response mechanisms which underlie these observations, including: I-A-regulated immunoselection against MuLV antigens expressed by (pre) leukaemic T cells, aberrant expression of class II MHC antigens on some B cell lymphomas and I-A-regulated chronic immunostimulation of MuLV-expressing (pre) leukaemic B cells, are discussed.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0305-1811
pubmed:author
pubmed:issnType
Print
pubmed:volume
13
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
69-76
pubmed:dateRevised
2003-11-14
pubmed:meshHeading
pubmed:articleTitle
The H-2 complex regulates both the susceptibility to mouse viral lymphomagenesis and the phenotype of the virus-induced lymphomas.
pubmed:publicationType
Journal Article, Review