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1996-03-09
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Document 0192
DOCN M9650192
TI Analysis of major histocompatibility complex class I-restricted hapten
recognition by mutation of the V-J joining of T cell receptor alpha
chains.
DT 9605
AU von Bonin A; Plaga S; Ruh H; Hebbelmann S; Pflugfelder U; Martin S;
Weltzien HU; Max-Planck-Institut fur Immunbiologie, Freiburg, Germany.
SO Eur J Immunol. 1996 Jan;26(1):179-86. Unique Identifier : AIDSLINE
MED/96152743
AB Hapten-specific T cell responses are responsible for chemically induced
immune disorders. However, the molecular details of hapten interactions
with T cell receptors (TCR) are poorly understood. Recent studies of
trinitrophenyl (TNP)-specific responses revealed major
histocompatibility complex-associated TNP-peptides as dominant epitopes
for CD8+ and CD4+ T cells. The present study is based on the observation
that two H-2Kb/TNP-specific CTL clones (II/7 and III/1), differing
exclusively in two amino acids of their TCR alpha chains, also differed
in their carrier specificities for various TNP-peptides. The genes of
the two alpha chains and the common beta chain were cloned into
expression vectors. Transfection of the TCR alpha chain of clone III/1
into a hybridoma of clone II/7 also transferred the fine specificity of
clone III/1, indicating that the small alpha chain variations were
indeed responsible for the different carrier specificities. Point
mutations bridging the difference between the alpha chains of clones
II/7 and III/1 and functional studies of the respective TCR alpha beta
transfectants into a TCR-negative hybridoma revealed an unexpected
result: the two receptors did not represent examples of structural
complementarity for different sets of hapten-peptide conjugates; rather,
they resembled two structures of principally similar specificity but of
significantly different overall affinity. This was demonstrated more
directly by comparing the fine specificities of III/1 transfectants
expressing or not expressing the co-receptor CD8: the CD8-negative III/1
transfectant assumed a specificity pattern indistinguishable from that
of a CD8-expressing, II/7-derived transfectant. Hence, comparable
alterations of antigen recognition may be induced either by subtle TCR
alterations or by removal of CD8, i.e. by the presence or absence of a
non-polymorphic adhesion molecule.
DE Amino Acid Sequence Animal Antigen Presentation/GENETICS Base
Sequence CD8-Positive T-Lymphocytes/PHYSIOLOGY Epitopes/GENETICS H-2
Antigens/*GENETICS/IMMUNOLOGY Haptens/*GENETICS/IMMUNOLOGY Hybridomas
Mice Molecular Sequence Data Mutagenesis, Site-Directed/*IMMUNOLOGY
Receptors, Antigen, T-Cell, alpha-beta/*GENETICS/IMMUNOLOGY Support,
Non-U.S. Gov't T-Lymphocytes, Cytotoxic/IMMUNOLOGY
Transfection/IMMUNOLOGY JOURNAL ARTICLE
SOURCE: National Library of Medicine. NOTICE: This material may be
protected by Copyright Law (Title 17, U.S.Code).