Enhanced delivery of exogenous peptides into the class I antigen processing and presentation pathway.
Infect Immun
; 70(6): 3249-58, 2002 Jun.
Article
in En
| MEDLINE
| ID: mdl-12011020
Current immunization strategies, using peptide or protein antigens, generally fail to elicit cytotoxic-T-lymphocyte responses, since these antigens are unable to access intracellular compartments where loading of major histocompatibility complex class I (MHC-I) molecules occurs. In an attempt to circumvent this, we investigated whether the GM1 receptor-binding B subunit of Escherichia coli heat-labile toxin (EtxB) could be used to deliver class I epitopes. When a class I epitope was conjugated to EtxB, it was delivered into the MHC-I presentation pathway in a GM1-binding-dependent fashion and resulted in the appearance of MHC-I-epitope complexes at the cell surface. Importantly, we show that the efficiency of EtxB-mediated epitope delivery could be strikingly enhanced by incorporating, adjacent to the class I epitope, a 10-amino-acid segment from the C terminus of the DNA polymerase (Pol) of herpes simplex virus. The replacement of this 10-amino-acid segment by a heterologous sequence or the introduction of specific amino acid substitutions within this segment either abolished or markedly reduced the efficiency of class I epitope delivery. If the epitope was extended at its C terminus, EtxB-mediated delivery into the class I presentation pathway was found to be completely dependent on proteasome activity. Thus, by combining the GM1-targeting function of EtxB with the 10-amino-acid Pol segment, highly efficient delivery of exogenous epitopes into the endogenous pathway of class I antigen processing and presentation can be achieved.
Full text:
1
Collection:
01-internacional
Database:
MEDLINE
Main subject:
Bacterial Toxins
/
Viral Proteins
/
T-Lymphocytes, Cytotoxic
/
Histocompatibility Antigens Class I
/
RNA-Binding Proteins
/
Antigen Presentation
/
Epitopes, T-Lymphocyte
/
Escherichia coli Proteins
/
Enterotoxins
Limits:
Animals
Language:
En
Journal:
Infect Immun
Year:
2002
Document type:
Article
Affiliation country:
United kingdom
Country of publication:
United States