title: Transfer of antigen from human B cells to dendritic cells.
abstract: The cooperation of B lymphocytes with other antigen presenting cells (APCs) is often necessary in the efficient processing and presentation of antigen. Herein, we describe a mechanism by which B cells physically interact with dendritic cells (DCs) resulting in the transfer of B cell receptor (BCR)-enriched antigen to these APCs. Antigen transfer involves direct contact between the two cells followed by the capture of B cell derived membrane and intracellular components. Strikingly, DCs acquire greater amounts of antigen by transfer from B cells than by endocytosis of free antigen. Blocking scavenger receptor A, a DC surface receptor involved in membrane acquisition, abrogates these events. We propose that antigen transfer from B cells to DCs results in a more focused immunologic response due to the selective editing of Ag by the BCR.
authors.affiliation: Section of Rheumatology, Department of Internal Medicine, Yale University School of Medicine, New Haven, CT 06520, USA.
authors.forename: Bohdan P
authors.initials: BP
authors.lastname: Harvey
authors.affiliation: Section of Rheumatology, Department of Internal Medicine, Yale University School of Medicine, New Haven, CT 06520, USA.
authors.forename: Maurice T
authors.initials: MT
authors.lastname: Raycroft
authors.affiliation: Section of Rheumatology, Department of Internal Medicine, Yale University School of Medicine, New Haven, CT 06520, USA.
authors.forename: Timothy E
authors.initials: TE
authors.lastname: Quan
authors.affiliation: Section of Rheumatology, Department of Internal Medicine, Yale University School of Medicine, New Haven, CT 06520, USA.
authors.forename: Benjamin J
authors.initials: BJ
authors.lastname: Rudenga
authors.affiliation: Section of Rheumatology, Department of Internal Medicine, Yale University School of Medicine, New Haven, CT 06520, USA.
authors.forename: Robert M
authors.initials: RM
authors.lastname: Roman
authors.affiliation: Section of Rheumatology, Department of Internal Medicine, Yale University School of Medicine, New Haven, CT 06520, USA.
authors.forename: Joe
authors.initials: J
authors.lastname: Craft
authors.affiliation: Section of Rheumatology, Department of Internal Medicine, Yale University School of Medicine, New Haven, CT 06520, USA. Electronic address: mark.mamula@yale.edu.
authors.forename: Mark J
authors.initials: MJ
authors.lastname: Mamula
mesh_terms: D017951:Antigen Presentation / Q000276:immunology*; D001402:B-Lymphocytes / Q000276:immunology*; D001692:Biological Transport / Q000276:immunology; D002450:Cell Communication / Q000276:immunology; D002478:Cells, Cultured; D003713:Dendritic Cells / Q000276:immunology*; D006801:Humans; D011947:Receptors, Antigen, B-Cell / Q000276:immunology*; D051117:Scavenger Receptors, Class A / Q000037:antagonists & inhibitors / Q000276:immunology*
chemical_list: D011947:Receptors, Antigen, B-Cell; D051117:Scavenger Receptors, Class A
keywords: AF488; Alexa Fluor(®) 488; Antigen presentation/processing; B cells; B lymphoblastoid cell line; B-LCL; CTFR; CTO; CellTrace™ Far Red; CellTracker™ Orange; Dendritic cells; IC; MdDC; MoDC; SR-A; Scavenger receptor A; TW; aIg; anti-human IgG/M F(ab′)2; class A scavenger receptor; immune complex; monocyte derived DC; myeloid DC; transwell