title: In vivo depletion of Thy-1-positive cells originating from normal bone marrow abrogates the suppression of gld disease in normal-gld mixed bone marrow chimeras.
abstract: Mice homozygous for gld develop an autoimmune syndrome characterized by hypergammaglobulinemia, massive accumulation of abnormal T cells and the production of autoantibodies. Previous studies in our laboratory have shown that reconstitution of lethally irradiated B6/gld recipients with a mixture of normal and gld bone marrow (BM) suppresses the gld-induced syndrome. In this report we extend this observation by demonstrating that the depletion of normal Thy-1+ cells, but not normal B cells, restores gld disease in mixed BM chimeras congenic for Thy-1 and IgH alleles. These results strongly suggest that normal T cells suppress the development of gld-related abnormalities. It is probable that the mechanism by which normal Thy-1+ cells mediate the suppression is Fas ligand dependent.
authors.affiliation: Department of Medicine, University of North Carolina, Chapel Hill 27599-7280.
authors.forename: G C
authors.initials: GC
authors.lastname: MacDonald
authors.forename: V N
authors.initials: VN
authors.lastname: Kakkanaiah
authors.forename: E S
authors.initials: ES
authors.lastname: Sobel
authors.forename: P L
authors.initials: PL
authors.lastname: Cohen
authors.forename: R A
authors.initials: RA
authors.lastname: Eisenberg
mesh_terms: D000818:Animals; D000954:Antigens, Surface / Q000235:genetics / Q000502:physiology*; D001323:Autoantibodies / Q000276:immunology; D001327:Autoimmune Diseases / Q000235:genetics / Q000276:immunology* / Q000628:therapy; D001402:B-Lymphocytes; D016026:Bone Marrow Transplantation / Q000276:immunology; D053222:Fas Ligand Protein; D006942:Hypergammaglobulinemia / Q000235:genetics / Q000276:immunology* / Q000628:therapy; D007143:Immunoglobulin Heavy Chains / Q000235:genetics / Q000276:immunology; D008212:Lymphocyte Depletion; D008232:Lymphoproliferative Disorders / Q000235:genetics / Q000276:immunology* / Q000628:therapy; D008562:Membrane Glycoproteins / Q000172:deficiency / Q000235:genetics / Q000502:physiology*; D051379:Mice; D008817:Mice, Mutant Strains / Q000235:genetics / Q000276:immunology*; D016853:Muromonab-CD3 / Q000276:immunology; D011828:Radiation Chimera; D012217:Rheumatoid Factor / Q000276:immunology; D050378:T-Lymphocytes, Regulatory / Q000276:immunology*; D018800:Thy-1 Antigens / Q000032:analysis; D019014:fas Receptor
chemical_list: D000954:Antigens, Surface; D001323:Autoantibodies; D053222:Fas Ligand Protein; C505658:Fasl protein, mouse; D007143:Immunoglobulin Heavy Chains; D008562:Membrane Glycoproteins; D016853:Muromonab-CD3; D018800:Thy-1 Antigens; D019014:fas Receptor; D012217:Rheumatoid Factor