Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
1983-12-17
pubmed:abstractText
Monoclonal antibody GK1.5 recognizes a determinant, designated L3T4a, on the murine T cell surface molecule L3T4. The expression of L3T4a by functional murine T cell clones appears to correlate primarily with class II MHC antigen reactivity rather than with functional phenotype. In previous studies, antigen-specific cytolysis by a cloned class II MHC antigen(I-Ak)-reactive CTL line was found to be blocked entirely by monoclonal antibody (mAb) GK1.5, at a step before the lethal hit. In the present studies, we demonstrate that mAb GK1.5 profoundly blocks antigen-specific proliferation and release of lymphokines by cloned murine class II MHC antigen-reactive helper T lymphocyte (HTL) lines. Analysis of cloned T cell hybridomas, however, suggests that there exists clonal heterogeneity in the degree of inhibition of class II MHC antigen-specific function by mAb GK 1.5. Finally, we present evidence that mAb GK1.5 blocks class II MHC antigen-specific function by blocking class II MHC antigen-specific binding. The data presented here lend considerable support to the concept both that L3T4 and the human Leu-3/T4 molecules are similar and that L3T4 plays a role in class II MHC antigen-reactivity by murine T cells.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
0022-1767
pubmed:author
pubmed:issnType
Print
pubmed:volume
131
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
2178-83
pubmed:dateRevised
2011-11-17
pubmed:meshHeading
pubmed:year
1983
pubmed:articleTitle
Evidence implicating L3T4 in class II MHC antigen reactivity; monoclonal antibody GK1.5 (anti-L3T4a) blocks class II MHC antigen-specific proliferation, release of lymphokines, and binding by cloned murine helper T lymphocyte lines.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't