Clec4A4 is a regulatory receptor for dendritic cells that impairs inflammation and T-cell immunity

Tomofumi Uto, Tomohiro Fukaya, Hideaki Takagi, Keiichi Arimura, Takeshi Nakamura, Naoya Kojima, Bernard Malissen and Katsuaki Sato ()
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Tomofumi Uto: Faculty of Medicine, University of Miyazaki
Tomohiro Fukaya: Faculty of Medicine, University of Miyazaki
Hideaki Takagi: Faculty of Medicine, University of Miyazaki
Keiichi Arimura: Faculty of Medicine, University of Miyazaki
Takeshi Nakamura: Faculty of Medicine, University of Miyazaki
Naoya Kojima: Tokai University
Bernard Malissen: Centre d'Immunologie de Marseille-Luminy, Université de la Méditerrannée, Case 906, Institut National de la Santé et de la Recherche Médicale U631, and Centre National de la Recherche Scientifique UMR6102
Katsuaki Sato: Faculty of Medicine, University of Miyazaki

Nature Communications, 2016, vol. 7, issue 1, 1-15

Abstract: Abstract Dendritic cells (DCs) comprise several subsets that are critically involved in the initiation and regulation of immunity. Clec4A4/DC immunoreceptor 2 (DCIR2) is a C-type lectin receptor (CLR) exclusively expressed on CD8α− conventional DCs (cDCs). However, how Clec4A4 controls immune responses through regulation of the function of CD8α− cDCs remains unclear. Here we show that Clec4A4 is a regulatory receptor for the activation of CD8α− cDCs that impairs inflammation and T-cell immunity. Clec4a4−/−CD8α− cDCs show enhanced cytokine production and T-cell priming following Toll-like receptor (TLR)-mediated activation. Furthermore, Clec4a4−/− mice exhibit TLR-mediated hyperinflammation. On antigenic immunization, Clec4a4−/− mice show not only augmented T-cell responses but also progressive autoimmune pathogenesis. Conversely, Clec4a4−/− mice exhibit resistance to microbial infection, accompanied by enhanced T-cell responses against microbes. Thus, our findings highlight roles of Clec4A4 in regulation of the function of CD8α− cDCs for control of the magnitude and quality of immune response.

Date: 2016
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DOI: 10.1038/ncomms11273

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