title: Plasmacytoid dendritic cells are crucial for the initiation of inflammation and T cell immunity in vivo.
abstract: Plasmacytoid dendritic cells (pDCs) are characterized as type I interferon-producing cells that engage endosomal toll-like receptors (TLRs) and exclusively express sialic acid binding Ig-like lectin (Siglec)-H. However, their role in vivo remains unclear. Here we report a critical role for pDCs in the regulation of inflammation and T cell immunity in vivo by using gene-targeted mice with a deficiency of Siglec-H and conditional ablation of pDCs. pDCs were required for inflammation triggered by a TLR ligand as well as by bacterial and viral infections. pDCs controlled homeostasis of effector and regulatory CD4(+) T cells. Upon antigenic stimulation and microbial infection, pDCs suppressed the induction of CD4(+) T cell responses and participated in the initiation of CD8(+) T cell responses. Furthermore, Siglec-H appeared to modulate the function of pDCs in vivo. Thus, our findings highlight previously unidentified roles of pDCs and the regulation of their function for the control of innate and adaptive immunity.
authors.affiliation: Laboratory for Dendritic Cell Immunobiology, RIKEN Research Center for Allergy and Immunology, 1-7-22 Suehiro-cho, Tsurumi-ku, Yokohama, Kanagawa 230-0045, Japan.
authors.forename: Hideaki
authors.initials: H
authors.lastname: Takagi
authors.forename: Tomohiro
authors.initials: T
authors.lastname: Fukaya
authors.forename: Kawori
authors.initials: K
authors.lastname: Eizumi
authors.forename: Yumiko
authors.initials: Y
authors.lastname: Sato
authors.forename: Kaori
authors.initials: K
authors.lastname: Sato
authors.forename: Azusa
authors.initials: A
authors.lastname: Shibazaki
authors.forename: Haruna
authors.initials: H
authors.lastname: Otsuka
authors.forename: Atsushi
authors.initials: A
authors.lastname: Hijikata
authors.forename: Takashi
authors.initials: T
authors.lastname: Watanabe
authors.forename: Osamu
authors.initials: O
authors.lastname: Ohara
authors.forename: Tsuneyasu
authors.initials: T
authors.lastname: Kaisho
authors.forename: Bernard
authors.initials: B
authors.lastname: Malissen
authors.forename: Katsuaki
authors.initials: K
authors.lastname: Sato
mesh_terms: D055011:Ablation Techniques; D000818:Animals; D000941:Antigens / Q000276:immunology; D001424:Bacterial Infections / Q000276:immunology; D015496:CD4-Positive T-Lymphocytes / Q000276:immunology; D018414:CD8-Positive T-Lymphocytes / Q000276:immunology; D003713:Dendritic Cells / Q000276:immunology* / Q000378:metabolism; D006561:Herpes Simplex / Q000276:immunology; D006706:Homeostasis / Q000276:immunology; D007111:Immunity, Cellular; D007249:Inflammation / Q000276:immunology* / Q000378:metabolism; D037102:Lectins / Q000172:deficiency / Q000235:genetics / Q000378:metabolism; D051379:Mice; D008810:Mice, Inbred C57BL; D010641:Phenotype; D011956:Receptors, Cell Surface / Q000172:deficiency / Q000235:genetics / Q000378:metabolism; D013601:T-Lymphocytes / Q000276:immunology*; D050378:T-Lymphocytes, Regulatory / Q000276:immunology; D058504:Th17 Cells / Q000276:immunology; D051193:Toll-Like Receptors / Q000378:metabolism
chemical_list: D000941:Antigens; D037102:Lectins; D011956:Receptors, Cell Surface; C510552:Siglech protein, mouse; D051193:Toll-Like Receptors