Graft-versus-host reaction and GvH disease.
Chronic GvHR was induced by inoculating parental lymphoid cells into F1 hybrid mouse. Combination of ATL and ATH, which were congenic recombinant strains differing only in H-2I and S region from each other, was chosen to induce class II-GvHR. Selective activation against partner's alloantigen of graft CD4+ T cells was the primary event of the GvHR and then led to concomitant activation of both graft and host cells. Immune dysregulation among these cells made the GvHR-mouse express various chronic diseases including immune complex glomerulonephritis, autoimmune-like lesions of the liver or the salivary gland, tumor-like proliferations of T cells and abnormal extramedullary hematopoiesis. Chronic GvHR was also induced by a preferential but not a selective activation of graft CD4+ T cells. A combination of DBA/2 and C57BL/6, which differ in whole MHC antigens, was an example. When D2 cells, but not B6 cells, were incoulated into the BDF1 mouse, predominant activation of CD4+ cells over CD8+ cells were observed. Contributing factors to this phenomenon were low responsiveness of graft CD8+ T cells to allogeneic class I MHC antigens and anti-parent activity of host CD8+ cells. Thus both graft and host cells participate either actively or passively in the reaction induced in the parent --> F1 experimental system of GvHR/D.
Harada
T
T
Department of Pathology I, Shimane Medical University, Izumo, Japan.
D000818:Animals; D015496:CD4-Positive T-Lymphocytes / Q000276:immunology / Q000637:transplantation; D018414:CD8-Positive T-Lymphocytes / Q000276:immunology; D017690:Cell Transplantation; D006086:Graft vs Host Disease / Q000276:immunology / Q000473:pathology; D006087:Graft vs Host Reaction / Q000276:immunology; D015395:Histocompatibility Antigens Class I / Q000276:immunology; D006824:Hybridization, Genetic; D007519:Isoantigens / Q000276:immunology; D008213:Lymphocyte Activation; D051379:Mice; D008815:Mice, Inbred Strains
D015395:Histocompatibility Antigens Class I; D007519:Isoantigens