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Differential T‐cell activation by B7‐1 expression
Author(s) -
Li Wei,
Rosenzweig Anthony,
Huber Brigitte T.
Publication year - 2003
Publication title -
immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.297
H-Index - 133
eISSN - 1365-2567
pISSN - 0019-2805
DOI - 10.1046/j.1365-2567.2003.01658.x
Subject(s) - t cell , antigen , biology , microbiology and biotechnology , major histocompatibility complex , peptide , adenoviridae , cell , t cell receptor , recombinant dna , immune system , immunology , biochemistry , gene
Summary T‐cell receptor‐mediated T‐cell activation requires cosimulation signal, which can be provided by B7‐1 molecule. Our previous study demonstrated that the coexpression of a covalent peptide/major histocompatibility complex class II molecule complex and costimulatory molecule B7‐1 by recombinant adenovirus leads to synergy in peptide‐specific T‐cell activation. However, the viral antigen‐specific T‐cell activation is not enhanced by B7‐1 expressed by the adenovirus. To verify the differential T cell activation by B7‐1 and investigate its underlying mechanisms, we constructed an adenovirus coexpressing a covalent complex of hen egg lysozyme peptide/I‐A k (HEL 46–61 /I‐A k ) and B7‐1 in the present study. In vivo studies revealed that HEL 46–61 ‐specific T‐cell response, but not viral antigen‐specific T‐cell response, was enhanced by B7‐1 expression mediated by the adenovirus, suggesting that exogenous B7‐1 expression may regulate T‐cell response to these two different antigens through distinct mechanisms. Furthermore, our results revealed that antigen‐presenting cells were unsusceptible to adenovirus infection in vivo . Based on these findings, the possible mechanism of differential B7‐1 costimulation on peptide‐specific and viral antigen‐specific T‐cell activation is discussed.