title: Immunodeficiency in graft-versus-host disease (GVHD). II. Effects of GVHD-induced suppressor cells on CD4+ T cell clones.
abstract: Lethally irradiated mice transplanted with H-2-matched, minor histocompatibility-disparate bone marrow develop graft-vs-host disease (GVHD) that is associated with severe immunodeficiency. Splenocytes from such mice contain radioresistant cells that profoundly suppress normal lymphocyte function. We now show that GVHD-induced suppressor cells also inhibit the proliferation of CD4+ T cell clones specific for different Ag and class II MHC determinants. These suppressors have a dominant anti-proliferative effect, because they inhibit DNA synthesis in response to receptor-mediated stimulation and growth-promoting lymphokines, without abolishing lymphokine secretion or lymphokine receptor expression by the cloned T cells. The implications of these findings, and the usefulness of T cell clones for studying immune suppression, are discussed.
authors.affiliation: Edward Mallinckrodt Department of Pediatrics, Washington University School of Medicine, St. Louis, MO 63110.
authors.forename: D A
authors.initials: DA
authors.lastname: Wall
authors.forename: S
authors.initials: S
authors.lastname: Hamberg
authors.forename: J L
authors.initials: JL
authors.lastname: Ferrara
authors.forename: A K
authors.initials: AK
authors.lastname: Abbas
mesh_terms: D000818:Animals; D000945:Antigens, Differentiation, T-Lymphocyte; D002999:Clone Cells / Q000276:immunology; D006086:Graft vs Host Disease / Q000276:immunology*; D007153:Immunologic Deficiency Syndromes / Q000276:immunology*; D008213:Lymphocyte Activation; D008222:Lymphokines / Q000096:biosynthesis; D051379:Mice; D008808:Mice, Inbred CBA; D010641:Phenotype; D015375:Receptors, Interleukin-2 / Q000378:metabolism; D006377:T-Lymphocytes, Helper-Inducer / Q000276:immunology* / Q000378:metabolism; D050378:T-Lymphocytes, Regulatory / Q000276:immunology*
chemical_list: D000945:Antigens, Differentiation, T-Lymphocyte; D008222:Lymphokines; D015375:Receptors, Interleukin-2