Editing Antigen Presentation: Antigen Transfer between Human B Lymphocytes and Macrophages Mediated by Class A Scavenger Receptors

• Published in: The Journal of immunology (1950) Vol. 181; no. 6; pp. 4043 - 4051
• Main Authors: Harvey, Bohdan P, Quan, Timothy E, Rudenga, Benjamin J, Roman, Robert M, Craft, Joe, Mamula, Mark J
• Format: Journal Article
• Language: English
• Published: United States Am Assoc Immnol 15.09.2008
• Subjects: Antigen Presentation - immunology; Antigen-Presenting Cells - immunology; Antigen-Presenting Cells - metabolism; B-Lymphocyte Subsets - immunology; B-Lymphocyte Subsets - metabolism; Cell Communication - immunology; Cell Line, Transformed; Cell Line, Tumor; Cell Membrane - immunology; Cell Membrane - metabolism; Coculture Techniques; Cytosol - immunology; Cytosol - metabolism; Humans; Macrophages - immunology; Macrophages - metabolism; Protein Transport - immunology; Receptors, Scavenger - classification; Receptors, Scavenger - physiology; Signal Transduction - immunology
• ISSN: 0022-1767; 1550-6606
• DOI: 10.4049/jimmunol.181.6.4043

B lymphocytes can function independently as efficient APCs. However, our previous studies demonstrate that both dendritic cells and macrophages are necessary to propagate immune responses initiated by B cell APCs. This finding led us to identify a process in mice whereby Ag-specific B cells transfer Ag to other APCs. In this study, we report the ability and mechanism by which human B lymphocytes can transfer BCR-captured Ag to macrophages. The transfer of Ag involves direct contact between the two cells followed by the capture of B cell-derived membrane and/or intracellular components by the macrophage. These events are abrogated by blocking scavenger receptor A, a receptor involved in the exchange of membrane between APCs. Macrophages acquire greater amounts of Ag in the presence of specific B cells than in their absence. This mechanism allows B cells to amplify or edit the immune response to specific Ag by transferring BCR-captured Ag to other professional APCs, thereby increasing the frequency of its presentation. Ag transfer may perpetuate chronic autoimmune responses to specific self-proteins and help explain the efficacy of B cell-directed therapies in human disease.