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Vaccination with T cell receptor peptides primes anti‐receptor cytotoxic T lymphocytes (CTL) and anergizes T cells specifically recognized by these CTL
Author(s) -
Kuhröber Andreas,
Schirmbeck Reinhold,
Reimann Jörg
Publication year - 1994
Publication title -
european journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.272
H-Index - 201
eISSN - 1521-4141
pISSN - 0014-2980
DOI - 10.1002/eji.1830240525
Subject(s) - ctl* , biology , cytotoxic t cell , epitope , t cell receptor , cd8 , microbiology and biotechnology , t cell , antigen , major histocompatibility complex , t lymphocyte , immunology , immune system , in vitro , biochemistry
Abstract We selected three peptides from the germ‐line sequence of the Vβ8.2 and Jβ2.3 gene segments of the murine T cell receptor for antigen (TCR) which contained putative K d ‐ and L d ‐restricted epitopes. Immunization of BALB/c (H‐2 d ) mice with the Vβ8.2(67–90) 23‐mer peptide 1 as well as the 15‐mer Vβ8.2(95–108)‐peptide 2 efficiently primed specific CD8 + cytotoxic T lymphocyte (CTL) responses in vivo against natural TCR‐Vβ8.2 epitopes. Vβ8.2 + T cells were not deleted in TCR peptide‐immunized mice because the fractions of Vβ8.2 + CD4 + and Vβ8.2 + CD8 + T cells in spleen and lymph nodes were not altered. The proliferative response of Vβ8.2 + T cells to stimulation by monoclonal antibody F23.2 was selectively suppressed (by 60–80%) in peptide‐immunized BALB/c mice, indicating partial anergy of this T subset. Immunization of BALB/c mice with the Jβ2.3‐derived peptide 3 stimulated a CD8 + CTL response against a class I‐restricted epitope within this Jβ segment that was also generated during natural “endogenous” processing of this self antigen. These data confirm the predictive value of major histocompatibility complex class I allele‐specific motifs. The described experiments indicate that TCR peptide‐primed CD8 + CTL recognize class I‐restricted, natural Vβ/Jβ‐TCR epitopes. Such anti‐TCR CTL may, thus, operate in Vβ‐specific immunoregulation of the T cell system suppressing their functional reactivity without deleting them.