Unconventional NK1.1(-) intermediate TCR cells as major T lymphocytes expanding in chronic graft-versus-host disease.
Chronic graft-versus-host disease (GVHD) accompanying autoimmune disease was induced in (C57BL/6xDBA/2) F(1) mice (H-2(b/d)) by an injection of splenic T cells of parental DBA/2 origin (H-2(d)). In parallel with the onset of proteinuria, an expansion of lymphocytes was induced in the liver and kidney, showing a peak at 2 weeks after the onset of disease. The majority of lymphocytes were of recipient origin (H-2(b/d)). The main lymphocyte subset among T cells at the pre-onset stage and after the onset of disease was CD8(+) NK1.1(-) CD3(int) cells (of extrathymic, hepatic origin) in both the liver and kidney. NK1.1(-) CD3(int) cells confer primarily neither NK-like nor NKT-like cytotoxicity. No induction of these types of cytotoxicity was observed in these mice with the expansion of NK1.1(-) CD3(int) cells. This raised the possibility that granulocytes induced in the liver and kidney might be associated with tissue damage. The present results suggest that, similarly to the case of autoimmune-prone mice with genetic background (e.g. MRL-lpr/lpr mice and BXSB mice), NK1.1(-) CD3(int) cells of extrathymic, hepatic origin might be crucial lymphocytes involved in the induction of the autoimmune-like disease in mice with chronic GVHD, in conjunction with Bcells (e.g. B-1 cells).
Miyakawa
Ryoko
R
Department of Immunology Niigata University School of Medicine, Japan.
Miyaji
Chikako
C
Watanabe
Hisami
H
Yokoyama
Hisashi
H
Tsukada
Chika
C
Asakura
Hitoshi
H
Abo
Toru
T
D019264:Adoptive Transfer; D000818:Animals; D000941:Antigens / Q000032:analysis*; D000950:Antigens, Ly; D000954:Antigens, Surface; D001323:Autoantibodies / Q000096:biosynthesis / Q000276:immunology; D001327:Autoimmune Diseases / Q000209:etiology / Q000276:immunology* / Q000473:pathology; D016175:B-Lymphocyte Subsets / Q000276:immunology; D017252:CD3 Complex / Q000032:analysis; D016516:CD4-CD8 Ratio; D018956:CD5 Antigens / Q000032:analysis; D018414:CD8-Positive T-Lymphocytes / Q000737:chemistry / Q000276:immunology / Q000637:transplantation; D002908:Chronic Disease; D003433:Crosses, Genetic; D003602:Cytotoxicity, Immunologic; D005260:Female; D006086:Graft vs Host Disease / Q000209:etiology / Q000276:immunology*; D006098:Granulocytes / Q000276:immunology / Q000473:pathology; D006183:H-2 Antigens / Q000276:immunology; D007072:Immunoglobulin D / Q000096:biosynthesis / Q000276:immunology; D007075:Immunoglobulin M / Q000096:biosynthesis / Q000276:immunology; D007668:Kidney / Q000276:immunology / Q000473:pathology; D007694:Killer Cells, Natural / Q000276:immunology*; D037181:Lectins, C-Type; D008099:Liver / Q000276:immunology / Q000473:pathology; D008213:Lymphocyte Activation; D008232:Lymphoproliferative Disorders / Q000209:etiology / Q000276:immunology*; D051379:Mice; D008810:Mice, Inbred C57BL; D008811:Mice, Inbred DBA; D019463:Mice, Inbred MRL lpr; D023421:Models, Animal; D055651:NK Cell Lectin-Like Receptor Subfamily B; D009393:Nephritis / Q000209:etiology / Q000276:immunology* / Q000473:pathology; D011506:Proteins / Q000032:analysis*; D011507:Proteinuria / Q000209:etiology; D013047:Specific Pathogen-Free Organisms; D013154:Spleen / Q000276:immunology; D016176:T-Lymphocyte Subsets / Q000737:chemistry / Q000276:immunology / Q000637:transplantation*
D000941:Antigens; D000950:Antigens, Ly; D000954:Antigens, Surface; D001323:Autoantibodies; D017252:CD3 Complex; D018956:CD5 Antigens; D006183:H-2 Antigens; D007072:Immunoglobulin D; D007075:Immunoglobulin M; C527211:Klrb1c protein, mouse; D037181:Lectins, C-Type; D055651:NK Cell Lectin-Like Receptor Subfamily B; D011506:Proteins