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PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
9
pubmed:dateCreated
1990-11-21
pubmed:abstractText
Cytotoxic T lymphocyte (CTL) clones against a syngeneic Friend virus-induced erythroleukemia (FBL-3) were generated in C57BL/6 (B6) mice. A monoclonal antibody (mAb, N9-127) was then raised from spleen cells of a B6 mouse immunized syngenically against one of these CTL clones. This mAb detected the epitope (127Ep) of the T cell antigen receptor (TcR) on the immunizing CTL clone in tests of immunoprecipitation, specific blocking and proliferation, and induction of TcR-mediated nonspecific lysis of the clone. In addition, more than 10% of the FBL-3-specific CTL clones isolated independently from B6 mice were 127Ep+. Further investigations revealed that up to 30% of B6 anti-FBL-3 T cell blasts from mixed lymphocyte tumor cell cultures were positive for this epitope, and that its expression was confined to CD8+ T cells. This epitope was not detected in naive lymphoid cells from the spleen, lymph nodes or thymus or in T cell clones specific for tumors other than FBL-3. The FBL-3-specific CTL clones were next grouped into 127Ep+ and 127Ep- clones. Sequence analyses of the CTL clone used for immunization showed the rearrangements of V alpha 1J alpha 112-2 and V beta 10D beta 2.1J beta 2.7. Southern blot analysis of all the 127Ep+ CTL clones examined showed the same DNA rearrangement bands of both the TcR alpha and beta genes. These findings suggested that mAb N9-127 recognized the shared determinant of the TcR molecule which was expressed by the dominant CTL population in the response to FBL-3.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
0014-2980
pubmed:author
pubmed:issnType
Print
pubmed:volume
20
pubmed:owner
NLM
pubmed:authorsComplete
N
pubmed:pagination
2095-103
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1990
pubmed:articleTitle
Participation of a dominant cytotoxic T cell population defined by a monoclonal antibody in syngeneic anti-tumor responses.
pubmed:affiliation
Institute for Immunology, Faculty of Medicine, Kyoto University, Japan.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't