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: Hideaki Takagi, Tomohiro Fukaya, Kawori Eizumi, Yumiko Sato, Kaori Sato, Azusa Shibazaki, Haruna Otsuka, Atsushi Hijikata, Takashi Watanabe, Osamu Ohara, Tsuneyasu Kaisho, Bernard Malissen, Katsuaki Sato
• Journal: Immunity (Immunity) Vol. 35 Issue 6 Pg. 958-71 (Dec 23 2011) ISSN: 1097-4180 [Electronic] United States
• PMID: 22177923 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
• Copyright: Copyright © 2011 Elsevier Inc. All rights reserved.

Chemical References

• Antigens
• Lectins
• Receptors, Cell Surface
• Siglech protein, mouse
• Toll-Like Receptors

Topics

• Ablation Techniques
• Animals
• Antigens (immunology)
• Bacterial Infections (immunology)
• CD4-Positive T-Lymphocytes (immunology)
• CD8-Positive T-Lymphocytes (immunology)
• Dendritic Cells (immunology, metabolism)
• Herpes Simplex (immunology)
• Homeostasis (immunology)
• Immunity, Cellular
• Inflammation (immunology, metabolism)
• Lectins (deficiency, genetics, metabolism)
• Mice
• Mice, Inbred C57BL
• Phenotype
• Receptors, Cell Surface (deficiency, genetics, metabolism)
• T-Lymphocytes (immunology)
• T-Lymphocytes, Regulatory (immunology)
• Th17 Cells (immunology)
• Toll-Like Receptors (metabolism)