Journal
NATURE COMMUNICATIONS
Volume 7, Issue -, Pages -Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/ncomms13277
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Funding
- US National Institutes of Health [R01NS098747, R01AI079293]
- Rede Mineira de Biomoleculas from Fundacao de Amparo a Pesquisa de Minas Gerais (Fapemig) [RED-00012-14]
- Brazilian National Institute of Science and Technology for Vaccines - Conselho Nacional de Desenvolvimento Cientifico e Tecnologico (CNPq)/Fapemig/Ministerio da Saude [573547/2008-4]
- Coordenacao de Aperfeicoamento de Pessoal de Ensino Superior (CAPES)
- David Rockefeller Center for Latin American Studies at Harvard University
- Science without Borders
- CNPq
- CAPES
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Dendritic cells have an important role in immune surveillance. After being exposed to microbial components, they migrate to secondary lymphoid organs and activate T lymphocytes. Here we show that during mouse malaria, splenic inflammatory monocytes differentiate into monocyte-derived dendritic cells (MO-DCs), which are CD11b(+)F4/80(+) CD11c(+)MHCII(high)DC-SIGN(high)Ly6c(+) and express high levels of CCR5, CXCL9 and CXCL10 (CCR5(+)CXCL9/10(+) MO-DCs). We propose that malaria-induced splenic MO-DCs take a reverse migratory route. After differentiation in the spleen, CCR5(+)CXCL9/10(+) MO-DCs traffic to the brain in a CCR2-independent, CCR5-dependent manner, where they amplify the influx of CD8(+) T lymphocytes, leading to a lethal neuropathological syndrome.
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