title: Suppression of xenogeneic graft-versus-host disease by treatment with immunoglobulin-like transcript 3-Fc.
abstract: Allogeneic hematopoietic cell transplantation represents an important therapy for certain malignant and nonmalignant diseases. However, graft-versus-host disease (GVHD) is a major cause of mortality and morbidity. The search for agents that can efficiently suppress GVHD has been going on for more than half a century. GVHD is particularly strong in xenogeneic donor-recipient combinations, given the unlimited number of potentially immunogenic antigens donor lymphocytes encounter in the host. Using a hu-nonobese diabetic/severe combined immunodeficiency (hu-NOD/SCID) gamma-null model of xenogeneic GVHD, we have demonstrated that treatment with recombinant immunoglobulin-like transcript 3-Fc protein induces the differentiation of CD8(+) T suppressor cells and blocks the cellular and humoral arm of the GVH reaction.
authors.affiliation: Department of Pathology, Columbia University, New York, NY 10032, USA.
authors.forename: George
authors.initials: G
authors.lastname: Vlad
authors.forename: Michael B
authors.initials: MB
authors.lastname: Stokes
authors.forename: Zhuoru
authors.initials: Z
authors.lastname: Liu
authors.forename: Chih-Chao
authors.initials: CC
authors.lastname: Chang
authors.forename: Hugo
authors.initials: H
authors.lastname: Sondermeijer
authors.forename: Elena R
authors.initials: ER
authors.lastname: Vasilescu
authors.forename: Adriana I
authors.initials: AI
authors.lastname: Colovai
authors.forename: Pasquale
authors.initials: P
authors.lastname: Berloco
authors.forename: Vivette D
authors.initials: VD
authors.lastname: D'Agati
authors.forename: Lloyd
authors.initials: L
authors.lastname: Ratner
authors.forename: Raffaello
authors.initials: R
authors.lastname: Cortesini
authors.forename: Nicole
authors.initials: N
authors.lastname: Suciu-Foca
mesh_terms: D000818:Animals; D000910:Antibodies, Heterophile / Q000276:immunology; D015478:Antigens, Heterophile / Q000276:immunology; D018414:CD8-Positive T-Lymphocytes / Q000276:immunology / Q000378:metabolism / Q000473:pathology; D002454:Cell Differentiation / Q000235:genetics; D018450:Disease Progression; D005260:Female; D005818:Genetic Engineering; D006086:Graft vs Host Disease / Q000276:immunology* / Q000503:physiopathology / Q000628:therapy; D018380:Hematopoietic Stem Cell Transplantation; D006801:Humans; D007141:Immunoglobulin Fc Fragments / Q000235:genetics / Q000276:immunology / Q000378:metabolism*; D007166:Immunosuppressive Agents / Q000276:immunology / Q000378:metabolism; D007167:Immunotherapy; D008562:Membrane Glycoproteins; D051379:Mice; D016688:Mice, Inbred NOD; D016513:Mice, SCID; D011828:Radiation Chimera; D011956:Receptors, Cell Surface / Q000235:genetics / Q000276:immunology / Q000378:metabolism*; D011971:Receptors, Immunologic; D011993:Recombinant Fusion Proteins / Q000235:genetics / Q000276:immunology / Q000378:metabolism*; D050378:T-Lymphocytes, Regulatory / Q000276:immunology / Q000378:metabolism / Q000473:pathology
chemical_list: D000910:Antibodies, Heterophile; D015478:Antigens, Heterophile; D007141:Immunoglobulin Fc Fragments; D007166:Immunosuppressive Agents; C107907:LILRB4 protein, human; D008562:Membrane Glycoproteins; D011956:Receptors, Cell Surface; D011971:Receptors, Immunologic; D011993:Recombinant Fusion Proteins