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Repertoires of T cell receptors specific for a single minor histocompatibility antigen during primary and recall CD8 T cell responses
Author(s) -
Choi Jung Hwa,
Ryu Su Jeong,
Jung Kyoung Min,
Chang Jun,
Choi Eun Young
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.2_supplement.534
Subject(s) - t cell receptor , cd8 , minor histocompatibility antigen , major histocompatibility complex , cytotoxic t cell , biology , t cell , epitope , antigen , immunology , immune system , microbiology and biotechnology , genetics , in vitro
Minor histocompatibility antigens (minor H Ags) are recognized by reactive CD8 T cells and induce immune responses after MHC‐matched transplantation. To understand the diversity of T cell receptor (TCR) repertoire in response to single minor H Ags, CDR3‐size spectratyping was used to study TCR repertoires participating in CD8 primary and recall responses to a dominant minor H Ag, H60. H60‐reactive CD8 T cells were purified, using H60‐peptide/MHC I tetramers, from splenocytes of C57BL/6 (B6) female mice immunized with H60 congenic splenocytes at the peak days of primary and secondary responses, days 10 and 7 postimmunization, respectively. The distribution patterns of CDR3‐size of the CD8 T cells showed skewed usages of specific sizes from diverse Vβ TCRs. Vβ5.2, Vβ 8.3, Vβ 11, and Vβ 16 were commonly found as dominant ones through the responses when HY‐derived CD4 and H60‐derived CD8 T cell epitopes were cognately presented. However, only a few Vβs were found to be used selectively and clonally expanded in the secondary response when HY‐derived CD4 and H60‐drived CD8 T cell epitopes were presented by separate cells. Our results suggest that appropriate provision of CD4 help will ensure CD8 T cells from diverse TCRs to react to H60. The data will be bases for generating TCR transgenic mice of which T cells have specificity for H60‐peptide/H‐2K b . * Supported by a KOSEF grant, R01‐2006‐10565‐0.