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¹ Department of Molecular Preventive Medicine and Solution Oriented Research for Science and Technology (SORST), Graduate School of Medicine, University of Tokyo, Bunkyo-ku, Tokyo 113-0033, Japan
² Department of Anatomy (Macro) and SORST, Dokkyo University School of Medicine, Tochigi 321-0293, Japan
³ Department of Pediatrics, Children's Hospital, Harvard Medical School, Boston, MA 02115

CORRESPONDENCE Kouji Matsushima: koujim{at}m.u-tokyo.ac.jp

Antiviral cell–mediated immunity is initiated by the dendritic cell (DC) network in lymph nodes (LNs). Plasmacytoid DCs (pDCs) are known to migrate to inflamed LNs and produce interferon (IFN)-, but their other roles in antiviral T cell immunity are unclear. We report that LN-recruited pDCs are activated to create local immune fields that generate antiviral cytotoxic T lymphocytes (CTLs) in association with LNDCs, in a model of cutaneous herpes simplex virus (HSV) infection. Although pDCs alone failed to induce CTLs, in vivo depletion of pDCs impaired CTL-mediated virus eradication. LNDCs from pDC-depleted mice showed impaired cluster formation with T cells and antigen presentation to prime CTLs. Transferring circulating pDC precursors from wild-type, but not CXCR3-deficient, mice to pDC-depleted mice restored CTL induction by impaired LNDCs. In vitro co-culture experiments revealed that pDCs provided help signals that recovered impaired LNDCs in a CD2- and CD40L-dependent manner. pDC-derived IFN- further stimulated the recovered LNDCs to induce CTLs. Therefore, the help provided by pDCs for LNDCs in primary immune responses seems to be pivotal to optimally inducing anti-HSV CTLs.

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