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Bright expression of CD 91 identifies highly activated human dendritic cells that can be expanded by defensins
Author(s) -
Cappelletti Monica,
Presicce Pietro,
Calcaterra Francesca,
Mavilio Domenico,
Della Bella Silvia
Publication year - 2015
Publication title -
immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.297
H-Index - 133
eISSN - 1365-2567
pISSN - 0019-2805
DOI - 10.1111/imm.12418
Subject(s) - cd80 , lipopolysaccharide , immune system , biology , microbiology and biotechnology , recombinant dna , in vitro , beta defensin , innate immune system , immunology , dendritic cell , cd40 , cytotoxic t cell , biochemistry , gene
Summary CD91 is a scavenger receptor expressed by different immune cells and its ligands defensins have been demonstrated to contribute to immune responses against infections and tumours. We previously demonstrated that CD91 is expressed on human monocyte‐derived dendritic cells (moDCs) and that human defensins stimulate in vitro the activation of these cells. In this study, we observed that CD91 is expressed at different levels on two distinct moDC subsets: CD91 dim and CD91 bright moDCs. Although CD91 bright moDCs represented a small proportion of total moDCs, this subset showed higher levels of activation and maturation markers compared with CD91 dim moDCs. The frequency of CD91 bright moDCs increased by ~ 50% after in vitro stimulation with recombinant human neutrophil peptide‐1 ( rHNP ‐1) and recombinant human β defensin‐1 ( rHBD ‐1), while lipopolysaccharide (LPS) stimulation decreased it by ~ 35%. Both defensins up‐regulated moDC expression of CD80, CD40, CD83 and HLA‐DR, although to a lower extent compared with LPS. Notably, upon culture with rHNP ‐1 and rHBD ‐1, CD91 bright moDCs maintained their higher activation/maturation status, whereas this was lost upon culture with LPS. Our findings suggest that defensins promote the differentiation into activated CD91 bright DCs and may encourage the exploitation of the CD91/defensins axis as a novel therapeutic strategy to potentiate antimicrobial and anti‐tumour immune response.