title: CX3CR1⁺ cells facilitate the activation of CD4 T cells in the colonic lamina propria during antigen-driven colitis.
abstract: Dendritic cells (DCs) and macrophages populate the intestinal lamina propria to initiate immune responses required for the maintenance of intestinal homeostasis. To investigate whether CX3CR1(+) phagocytes communicate with CD4 T cells during the development of transfer colitis, we established an antigen-driven colitis model induced by the adoptive transfer of DsRed OT-II cells in CX3CR1(GFP/+) × RAG(-/-) recipients challenged with Escherichia coli expressing ovalbumin (OVA) fused to a cyan fluorescent protein (CFP). After colonization of CX3CR1(GFP/+) × RAG(-/-) animals with red fluorescent E. coli pCherry-OVA, colonic CX3CR1(+) cells but not CD103(+) DCs phagocytosed E. coli pCherry-OVA. Degraded bacterial-derived antigens are transported by CD103(+) DCs to mesenteric lymph nodes (MLNs), where CD103(+) DCs prime naive T cells. In RAG(-/-) recipients reconstituted with OT II cells and gavaged with OVA-expressing E. coli, colonic CX3CR1(+) phagocytes are in close contact with CD4 T cells and presented bacterial-derived antigens to CD4 T cells to activate and expand effector T cells.
authors.affiliation: Department of Internal Medicine I, Ulm University, Ulm, Germany.
authors.forename: V
authors.initials: V
authors.lastname: Rossini
authors.affiliation: Institute of Microbiology and Biotechnology, Ulm University, Ulm, Germany.
authors.forename: D
authors.initials: D
authors.lastname: Zhurina
authors.affiliation: Department of Internal Medicine I, Ulm University, Ulm, Germany.
authors.forename: K
authors.initials: K
authors.lastname: Radulovic
authors.affiliation: Department of Internal Medicine I, Ulm University, Ulm, Germany.
authors.forename: C
authors.initials: C
authors.lastname: Manta
authors.affiliation: Electron Microscopy Facility, Ulm University, Ulm, Germany.
authors.forename: P
authors.initials: P
authors.lastname: Walther
authors.affiliation: Institute of Microbiology and Biotechnology, Ulm University, Ulm, Germany.
authors.forename: C U
authors.initials: CU
authors.lastname: Riedel
authors.affiliation: 1] Department of Internal Medicine I, Ulm University, Ulm, Germany [2] Department of Visceral Medicine and Surgery, Division of Gastroenterology, Inselspital, Bern, Switzerland.
authors.forename: J H
authors.initials: JH
authors.lastname: Niess
mesh_terms: D000818:Animals; D000941:Antigens / Q000276:immunology; D015703:Antigens, CD / Q000378:metabolism; D015496:CD4-Positive T-Lymphocytes / Q000276:immunology*; D000073883:CX3C Chemokine Receptor 1; D003092:Colitis / Q000235:genetics / Q000276:immunology* / Q000378:metabolism* / Q000473:pathology; D003713:Dendritic Cells / Q000276:immunology / Q000378:metabolism; D004195:Disease Models, Animal; D004926:Escherichia coli / Q000276:immunology; D005260:Female; D039001:Integrin alpha Chains / Q000378:metabolism; D007413:Intestinal Mucosa / Q000276:immunology* / Q000378:metabolism* / Q000382:microbiology / Q000473:pathology; D008198:Lymph Nodes / Q000276:immunology / Q000378:metabolism; D008213:Lymphocyte Activation / Q000276:immunology*; D008297:Male; D008643:Mesentery; D051379:Mice; D018345:Mice, Knockout; D010047:Ovalbumin / Q000276:immunology; D010586:Phagocytes / Q000276:immunology / Q000378:metabolism; D010641:Phenotype; D019707:Receptors, Chemokine / Q000235:genetics / Q000378:metabolism*; D037182:T-Cell Antigen Receptor Specificity / Q000276:immunology
chemical_list: D000941:Antigens; D015703:Antigens, CD; D000073883:CX3C Chemokine Receptor 1; C471885:Cx3cr1 protein, mouse; D039001:Integrin alpha Chains; D019707:Receptors, Chemokine; C091367:alpha E integrins; D010047:Ovalbumin