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V Bierre

Publications and source records attributed to V Bierre.

8 recordsLinked to original sources
PubMed1994

Split tolerance in chimeric GVH mice.

The i.v. inoculation of parental spleen cells into unirradiated adult F1 hybrid mice results in a graft-versus-host reaction (GVHR). In the strain combination B10D2 --> (B10.BRx B10.D2) F1, this reaction is associated with thymic injury and transient but profound cellular immune deficiency. We further analysed the immune status of these mice 60 days after GVHR induction. Phenotypic studies of spleen cells showed that these mice were repopulated with parental lymphocytes resulting in a high degree of chimerism (85%). At this time, the mice looked healthy and recovered a normal cytotoxic T cell response (CTL) against allogeneic cells. GVH chimeric splenocytes were unresponsive against F1 hybrid cells in mixed lymphocyte culture (MLC), but exhibited anti-F1 CTL reactivity. We also analysed the anti-F1 reactivity of these mice in vivo. GVH chimeric splenocytes were unable to induce GVHR after injection into a new F1 hybrid and F1 GVH mice specifically rejected F1 bone marrow (BM) cells after lethal irradiation. Grafting a neonatal parental thymus prevented the rejection of F1 BM cells and restored CTL alloreactivity. It is concluded that the chimeric state induced by GVHR is associated with a split tolerance and that a radiosensitive thymic-dependent mechanism is involved in maintaining self-tolerance in these mice.

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PubMed1992

Absence of correlation between graft-versus-host associated immunosuppression and cytotoxic T cell activity in response to major histocompatibility antigens.

Studies in mice suggest that the T cell subset involved in graft-versus-host-reaction (GvHR) across the major histocompatibility complex (MHC) depends on the class of MHC antigens recognized by the donor cells. However, the correlation between phenotype and function is not absolute. Using a functional approach, we investigated in a parent --> F1 hybrid model differing at the whole MHC, whether graft-versus-host (GvH) associated immunosuppression was correlated with donor cytotoxic T cell activity. The immunodeficiency was tested by the ability of the F1 mice to generate a cytotoxic T cell response against trinitrophenyl-modified syngeic cells (TNF-self) or an alloantigen. F1 specific parental cytotoxic T cells, generated in vitro, induced less immunosuppression than naive parental cells. Specific in vivo priming increased the cytotoxicity of parental spleen cells, but decreased their capacity to induce GvH-associated immunosuppression. In contrast, nonspecific priming resulted in the usual immunodeficiency. In conclusion, there was no correlation between GvH-associated immunosuppression and cytotoxic T cell activity of the parental cells.

Animals↗
PubMed1991

[Immune deficiency associated with experimental graft-versus-host reaction. Lack of correlation with T-cell cytotoxic activity].

Graft-versus-host reactions (GvHR) are initiated by T lymphocytes. In mice, the T cell subset involved depends on the incompatibility for minor or major histocompatibility antigens between donor and host. However, the correlation between phenotype and function is not absolute, and anti-host cytotoxic T cells can be detected in recipients without GvHR. We have presently investigated in a P----F1 model differing at the MHC, whether GvH associated immunosuppression was correlated with donor cytotoxic T cell activity. The immunodeficiency was tested by the ability of the F1 mice to generate a cytotoxic T cell response against TNP self or an alloantigen. F1 specific parental cytotoxic T cells generated in vitro induced less immunosuppression than naive parental spleen cells. Specific in vivo priming increased the cytotoxicity of parental spleen cells, but decreased their capacity to induce GvH associated immunosuppression. In contrast, non specific priming resulted the usual immunodeficiency. Spleens of the F1 mice injected with specific cytotoxic T cells were very enlarged, suggesting that these cells remained capable of inducing a GvHR without generating immunosuppression.

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