title: Murine CD83-positive T cells mediate suppressor functions in vitro and in vivo.
abstract: The CD83 molecule (CD83) is a well-known surface marker present on mature dendritic cells (mDC). In this study, we show that CD83 is also expressed on a subset of T cells which mediate regulatory T cell (Treg)-like suppressor functions in vitro and in vivo. Treg-associated molecules including CD25, cytotoxic T lymphocyte antigen-4 (CTLA-4), glucocorticoid-induced TNFR family-related gene (GITR), Helios and neuropilin-1 (NRP-1) as well as forkhead box protein 3 (FOXP3) were specifically expressed by these CD83(+) T cells. In contrast, CD83(-) T cells showed a naive T cell phenotype with effector T cell properties upon activation. Noteworthy, CD83(-) T cells were not able to upregulate CD83 despite activation. Furthermore, CD83(+) T cells suppressed the proliferation and inflammatory cytokine release of CD83(-) T cells in vitro. Strikingly, stimulated CD83(+) T cells released soluble CD83 (sCD83), which has been reported to possess immunosuppressive properties. In vivo, using the murine transfer colitis model we could show that CD83(+) T cells were able to suppress colitis symptoms while CD83(-) T cells possessed effector functions. In addition, this CD83 expression is also conserved on expanded human Treg. Thus, from these studies we conclude that CD83(+) T cells share important features with regulatory T cells, identifying CD83 as a novel lineage marker to discriminate between different T cell populations.
authors.affiliation: Department of Immune Modulation at the Department of Dermatology, University Hospital Erlangen, Erlangen D-91052, Germany.
authors.forename: Simon
authors.initials: S
authors.lastname: Kreiser
authors.affiliation: Department of Immune Modulation at the Department of Dermatology, University Hospital Erlangen, Erlangen D-91052, Germany.
authors.forename: Jenny
authors.initials: J
authors.lastname: Eckhardt
authors.affiliation: Department of Immune Modulation at the Department of Dermatology, University Hospital Erlangen, Erlangen D-91052, Germany.
authors.forename: Christine
authors.initials: C
authors.lastname: Kuhnt
authors.affiliation: Department of Immune Modulation at the Department of Dermatology, University Hospital Erlangen, Erlangen D-91052, Germany.
authors.forename: Marcello
authors.initials: M
authors.lastname: Stein
authors.affiliation: Department of Immune Modulation at the Department of Dermatology, University Hospital Erlangen, Erlangen D-91052, Germany.
authors.forename: Lena
authors.initials: L
authors.lastname: Krzyzak
authors.affiliation: Department of Immune Modulation at the Department of Dermatology, University Hospital Erlangen, Erlangen D-91052, Germany.
authors.forename: Christine
authors.initials: C
authors.lastname: Seitz
authors.affiliation: Department of Immune Modulation at the Department of Dermatology, University Hospital Erlangen, Erlangen D-91052, Germany.
authors.forename: Christine
authors.initials: C
authors.lastname: Tucher
authors.affiliation: Department of Immune Modulation at the Department of Dermatology, University Hospital Erlangen, Erlangen D-91052, Germany.
authors.forename: Ilka
authors.initials: I
authors.lastname: Knippertz
authors.affiliation: Department of Medicine 1, University Hospital Erlangen, Erlangen D-91052, Germany.
authors.forename: Christoph
authors.initials: C
authors.lastname: Becker
authors.affiliation: Department of Medicine 1, University Hospital Erlangen, Erlangen D-91052, Germany.
authors.forename: Claudia
authors.initials: C
authors.lastname: Günther
authors.affiliation: Department of Immune Modulation at the Department of Dermatology, University Hospital Erlangen, Erlangen D-91052, Germany.
authors.forename: Alexander
authors.initials: A
authors.lastname: Steinkasserer
authors.affiliation: Department of Immune Modulation at the Department of Dermatology, University Hospital Erlangen, Erlangen D-91052, Germany; Department of Medicine 1, University Hospital Erlangen, Erlangen D-91052, Germany. Electronic address: matthias.lechmann@uk-erlangen.de.
authors.forename: Matthias
authors.initials: M
authors.lastname: Lechmann
mesh_terms: D000818:Animals; D015703:Antigens, CD / Q000097:blood / Q000235:genetics / Q000378:metabolism*; D003092:Colitis / Q000235:genetics / Q000276:immunology / Q000378:metabolism; D016207:Cytokines / Q000096:biosynthesis; D004195:Disease Models, Animal; D015870:Gene Expression; D018398:Homeodomain Proteins / Q000235:genetics; D006801:Humans; D007136:Immunoglobulins / Q000097:blood / Q000235:genetics / Q000378:metabolism*; D007156:Immunologic Memory; D056747:Immunomodulation; D016130:Immunophenotyping; D008213:Lymphocyte Activation / Q000235:genetics / Q000276:immunology; D008562:Membrane Glycoproteins / Q000097:blood / Q000235:genetics / Q000378:metabolism*; D051379:Mice; D018345:Mice, Knockout; D008822:Mice, Transgenic; D010641:Phenotype; D016176:T-Lymphocyte Subsets / Q000276:immunology* / Q000378:metabolism*; D050378:T-Lymphocytes, Regulatory / Q000276:immunology / Q000378:metabolism; D000097802:CD83 Antigen
chemical_list: D015703:Antigens, CD; D016207:Cytokines; D018398:Homeodomain Proteins; D007136:Immunoglobulins; D008562:Membrane Glycoproteins; D000097802:CD83 Antigen; C064658:RAG-1 protein
keywords: CD83; Suppression; T cell; Transfer colitis; Treg