Document Detail

Analysis of major histocompatibility complex class I-restricted hapten recognition by mutation of the V-J joining of T cell receptor alpha chains.
MedLine Citation:
PMID:  8566064     Owner:  NLM     Status:  MEDLINE    
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.
A von Bonin; S Plaga; H Ruh; S Hebbelmann; U Pflugfelder; S Martin; H U Weltzien
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  European journal of immunology     Volume:  26     ISSN:  0014-2980     ISO Abbreviation:  Eur. J. Immunol.     Publication Date:  1996 Jan 
Date Detail:
Created Date:  1996-03-06     Completed Date:  1996-03-06     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  1273201     Medline TA:  Eur J Immunol     Country:  GERMANY    
Other Details:
Languages:  eng     Pagination:  179-86     Citation Subset:  IM; X    
Max-Planck-Institut für Immunbiologie, Freiburg, Germany.
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MeSH Terms
Amino Acid Sequence
Antigen Presentation / genetics
Base Sequence
CD8-Positive T-Lymphocytes / physiology
Epitopes / genetics
H-2 Antigens / genetics*,  immunology
Haptens / genetics*,  immunology
Molecular Sequence Data
Mutagenesis, Site-Directed / immunology*
Receptors, Antigen, T-Cell, alpha-beta / genetics*,  immunology
T-Lymphocytes, Cytotoxic / immunology
Transfection / immunology
Reg. No./Substance:
0/Epitopes; 0/H-2 Antigens; 0/H-2Kb protein, mouse; 0/Haptens; 0/Receptors, Antigen, T-Cell, alpha-beta

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