[The influence of subclinical level of graft versus host reaction on reconstitution of host lymphoid tissues].
In this study reconstitution of lymphoid tissues under the influence of subclinical graft versus host reaction (GVHR) was investigated. Lethally irradiated recipient mice (AKR: H-2k, Mls-1a) were reconstituted with donor (B10: H-2b, Mls-1b) bone marrow (BM) cells treated with anti-Thy 1 antibody alone without complement (GVHR chimeras). When their immunological reconstitution was analysed and compared with that of AKR recipients which had been reconstituted with B10 BM treated with anti-Thy 1 and complement (Control chimera), both of these chimeras all survived more than 100 days without showing clinical signs of GVHD. Full donor chimerism was accomplished at an early stage after BM transplantation (BMT) in GVHR chimeras, whereas substantial number of recipient T cells persisted in Control chimeras during the entire observation period. No significant difference was observed in the reconstitution of the thymus and spleen between the Control and GVHR chimeras. By contrast, the reconstitution of lymph nodes (LN) in GVHR chimeras was inhibited. The apparent failure of LN reconstitution was attributed to damage of LN structure involved in homing of lymphocytes, but not attributable to damage of lymphocytes themselves. Since donor CD8+ T cells caused the damage, target antigens of this damage appeared to be H-2 class I molecules in the present system. Furthermore, clonal deletion of V beta 6+T cells that are reactive to recipient Mls-1a antigen was induced in Control chimeras but abrogated in the GVHR chimeras. The latter abrogation of clonal deletion of V beta 6+T cells appeared to result from the early disappearance of recipient T cells in these GVHR chimeras.
Hirano
M
M
Third Department of Internal Medicine, Hokkaido University School of Medicine, Sapporo, Japan.
D000818:Animals; D016026:Bone Marrow Transplantation; D016516:CD4-CD8 Ratio; D002678:Chimera; D017637:Clonal Deletion; D006087:Graft vs Host Reaction / Q000276:immunology*; D008221:Lymphoid Tissue / Q000276:immunology*; D051379:Mice; D008806:Mice, Inbred AKR; D008810:Mice, Inbred C57BL; D013601:T-Lymphocytes