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Cytotoxic T lymphocyte recognition of a xenogeneic major histocompatibility complex antigen expressed in transgenic mice
Author(s) -
Bluestone Jeffrey A.,
Pescovitz Mark D.,
Frels William I.,
Singer Dinah S.,
Hodes Richard J.
Publication year - 1987
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.1830170721
Subject(s) - biology , cytotoxic t cell , histocompatibility , major histocompatibility complex , immunology , transgene , antigen , minor histocompatibility antigen , genetically modified mouse , gene , genetics , human leukocyte antigen , in vitro
Abstract Introduction of a porcine major histocompatability complex (MHC) class I gene (PD1) into the genome of a C57BL/10 (B10) mouse has been shown to lead to cell surface expression of the porcine MHC antigen, SLA PD1 in a transgenic mouse. The PD1 product expressed on spleen cells from the transgenic mice stimulated B10 spleen cells in a mixed lymphocyte culture to generate PD1‐specific cytotoxic T lymphocytes (CTL). The CTL were PD1 specific since they lysed transgenic splenic blast cells and PD1‐transfected L cells, but not B10 blasts or control L cells. The CTL were L3T4 − , Lyt‐2 + and their activity was partially inhibited by either anti‐Lyt‐2 antibody or by anti‐swine MHC alloantibodies. The repertoire of responding B10 anti‐transgenic CTL was assessed by examining their cross‐reactivity on a series of murine allogeneic targets. The B10 anti‐transgenic CTL showed some cross‐reactivity on conventional allogeneic targets, but reacted strongly on a series of mutant H‐2K bm blast cells. In addition, B10 anti‐B6.cH‐2 bm6 CTL cross‐reacted extensively on the transgenic target cells. These results demonstrated that normal B10 CTL possess a repertoire specific for the products of the xenogeneic class I gene PD1, that this repertoire is cross‐reactive with the conventional alloreactive CTL repertoire, and that there exists an unanticipated relationship between PD1‐specific CTL and CTL specific for K b mutant determinants.