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Host‐Reactive Cytotoxic T Lymphocyte Precursors in Long‐lived Fully Allogeneic Mouse Bone Marrow Chimeras
Author(s) -
HEEG K.,
REIMANN J.,
HEIT H.,
HEIT W.,
WAGNER H.
Publication year - 1986
Publication title -
scandinavian journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.934
H-Index - 88
eISSN - 1365-3083
pISSN - 0300-9475
DOI - 10.1111/j.1365-3083.1986.tb01959.x
Subject(s) - ctl* , chimera (genetics) , cytotoxic t cell , immunology , bone marrow , biology , spleen , antigen , graft versus host disease , stem cell , cd8 , microbiology and biotechnology , in vitro , genetics , gene
Fully H‐2‐incompatible chimeric mice were constructed by grafting lethally (950 rad) irradiated germ‐free (GF) CBA (H2 k ) mice with anti‐Thy 1 antibody plus complement‐treated allogeneic C57B1/6 (B6) (H2 b ) bone marrow cells. These chimeric mice were kept for more than 11 months, either under GF conditions or under barrier‐sustained specific‐pathogen‐free (SPF) conditions. Controls included nonirradiated, nontransplanted, sex‐ and age‐matched CBA and B6 mice raised under SPF conditions, and syngeneic chimeric mice of the CBA × CBA type kept under GF and SPF conditions. All chimeric mice were completely repopulated with donor‐type lymphoid cells and showed no clinical or histological evidence of graft‐versus‐host disease. From the fully allogeneic chimeric mice, we enumerated the numbers of splenic cytotoxic T lymphocyte precursors (CTL‐p) that could be clonally expanded under limiting dilution conditions in response to third‐party alloantigens, or nonmodified and trinitrophenyl (TNP)‐modified stimulator cells bearing host or donor H‐2 antigens. The existence of high numbers of alloreactive and host‐ or donor‐type H‐2‐restricted TNP‐specific CTL‐p in the spleens of fully allogeneic chimeras indicated almost normal immunocompetence. The surprising finding, however, was that large numbers of host (CBA)‐reactive splenic CTL‐p were inducible under limiting dilution conditions in healthy long‐lived allogeneic chimeras, although these chimeric mice were devoid of any histological or clinical signs of graft‐versus‐host disease.