title: Monocyte-Derived Dendritic Cells Promote Th Polarization, whereas Conventional Dendritic Cells Promote Th Proliferation.
abstract: Monocyte-derived dendritic cells (moDCs) dramatically increase in numbers upon infection and inflammation; accordingly, we found that this also occurs during allogeneic responses. Despite their prominence, how emergent moDCs and resident conventional DCs (cDCs) divide their labor as APCs remain undefined. Hence, we compared both direct and indirect presentation by murine moDCs versus cDCs. We found that, despite having equivalent MHC class II expression and in vitro survival, moDCs were 20-fold less efficient than cDCs at inducing CD4(+) T cell proliferation through both direct and indirect Ag presentation. Despite this, moDCs were more potent at inducing Th1 and Th17 differentiation (e.g., 8-fold higher IFN-γ and 2-fold higher IL-17A in T cell cocultures), whereas cDCs induced 10-fold higher IL-2 production. Intriguingly, moDCs potently reduced the ability of cDCs to stimulate T cell proliferation in vitro and in vivo, partially through NO production. We surmise that such division of labor between moDCs and cDCs has implications for their respective roles in the immune response.
authors.affiliation: Immunology Division, Walter and Eliza Hall Institute of Medical Research, Parkville, Victoria 3052, Australia; Department of Medical Biology, University of Melbourne, Parkville, Victoria 3010, Australia; Department of Nephrology, Royal Melbourne Hospital, Parkville, Victoria 3050, Australia; and.
authors.forename: Kevin V
authors.initials: KV
authors.lastname: Chow
authors.affiliation: Immunology Division, Walter and Eliza Hall Institute of Medical Research, Parkville, Victoria 3052, Australia; Department of Medical Biology, University of Melbourne, Parkville, Victoria 3010, Australia; Department of Microbiology and Immunology, University of Melbourne, Parkville, Victoria 3010, Australia lew@wehi.edu.au zhan@wehi.edu.au.
authors.forename: Andrew M
authors.initials: AM
authors.lastname: Lew
authors.affiliation: Immunology Division, Walter and Eliza Hall Institute of Medical Research, Parkville, Victoria 3052, Australia; Department of Medical Biology, University of Melbourne, Parkville, Victoria 3010, Australia;
authors.forename: Robyn M
authors.initials: RM
authors.lastname: Sutherland
authors.affiliation: Immunology Division, Walter and Eliza Hall Institute of Medical Research, Parkville, Victoria 3052, Australia; Department of Medical Biology, University of Melbourne, Parkville, Victoria 3010, Australia; lew@wehi.edu.au zhan@wehi.edu.au.
authors.forename: Yifan
authors.identifier: http://orcid.org/0000-0001-6974-0486
authors.initials: Y
authors.lastname: Zhan
mesh_terms: D000818:Animals; D017951:Antigen Presentation / Q000276:immunology; D002454:Cell Differentiation / Q000276:immunology*; D019070:Cell Lineage; D049109:Cell Proliferation; D018920:Coculture Techniques; D003713:Dendritic Cells / Q000166:cytology* / Q000276:immunology*; D005434:Flow Cytometry; D008213:Lymphocyte Activation / Q000276:immunology*; D051379:Mice; D008807:Mice, Inbred BALB C; D008810:Mice, Inbred C57BL; D008822:Mice, Transgenic; D009000:Monocytes / Q000166:cytology*; D006377:T-Lymphocytes, Helper-Inducer / Q000166:cytology / Q000276:immunology*