| Literature DB >> 31231033 |
Dong Liu1, Xiangyun Yin1, Sam J Olyha1, Manuela Sales L Nascimento2, Pei Chen3, Theresa White4, Uthaman Gowthaman1, Tingting Zhang5, Jake A Gertie1, Biyan Zhang1, Lan Xu1, Marina Yurieva6, Lesley Devine7, Adam Williams8, Stephanie C Eisenbarth9.
Abstract
Type 1 CD8α+ conventional dendritic cells (cDC1s) are required for CD8+ T cell priming but, paradoxically, promote splenic Listeria monocytogenes infection. Using mice with impaired cDC2 function, we ruled out a role for cDC2s in this process and instead discovered an interleukin-10 (IL-10)-dependent cellular crosstalk in the marginal zone (MZ) that promoted bacterial infection. Mice lacking the guanine nucleotide exchange factor DOCK8 or CD19 lost IL-10-producing MZ B cells and were resistant to Listeria. IL-10 increased intracellular Listeria in cDC1s indirectly by reducing inducible nitric oxide synthase expression early after infection and increasing intracellular Listeria in MZ metallophilic macrophages (MMMs). These MMMs trans-infected cDC1s, which, in turn, transported Listeria into the white pulp to prime CD8+ T cells. However, this also facilitated bacterial expansion. Therefore, IL-10-mediated crosstalk between B cells, macrophages, and cDC1s in the MZ promotes both Listeria infection and CD8+ T cell activation.Entities:
Keywords: DOCK8; IL-10; Listeria monocytogenes; T cell; dendritic cells; iNOS; macrophage; marginal zone B cells; spleen
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Year: 2019 PMID: 31231033 PMCID: PMC6685086 DOI: 10.1016/j.immuni.2019.05.011
Source DB: PubMed Journal: Immunity ISSN: 1074-7613 Impact factor: 31.745