Lost therapeutic potential of monocyte-derived dendritic cells through lost tissue homing: Stable restoration of gut specificity with retinoic acid
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Authors
Bernardo, DMann, ER
Al-Hassi, HO
English, NR
Man, R
Lee, GH
Ronde, E
Landy, J
Peake, STC
Hart, AL
Knight, SC
Issue Date
2013-09-08
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Show full item recordAbstract
Summary: Human monocyte-derived dendritic cells (DC) (MoDC) are utilized for immunotherapy. However, in-vitro immunological effects are often not mirrored in vivo. We studied the tissue-homing potential of MoDC. Circulating monocytes and DC expressed different tissue-homing markers and, during in-vitro development of MoDC, homing marker expression was lost resulting in a 'homeless' phenotype. Retinoic acid (RA) induced gut-homing markers (β7 and CCR9) and a regulatory phenotype and function [decreased human leucocyte antigen D-related (HLA-DR) and increased ILT3 and fluorescein isothiocyanate (FITC-dextran uptake) in MoDC]. RA-MoDC were less stimulatory and primed conditioned T cells with a gut-homing profile (β7+CLA-). Unlike the normal intestinal microenvironment, that from inflamed colon of ulcerative colitis (UC) patients did not induce regulatory properties in MoDC. However, RA-MoDC maintained their regulatory gut-specific properties even in the presence of UC microenvironment. Therefore, MoDC may be ineffectual for immunotherapy because they lack tissue-homing and tissue-imprinting specificity. However, MoDC rehabilitation with gut-homing potential by RA could be useful in promoting immunotherapy in pathologies such as UC. © 2013 The Authors. Clinical and Experimental Immunology published by John Wiley & Sons Ltd on behalf of British. Society for Immunology.Citation
Bernardo, D., Mann, E.R., Al-Hassi, H.O. et al (2013) Lost therapeutic potential of monocyte-derived dendritic cells through lost tissue homing: Stable restoration of gut specificity with retinoic acid, Clinical and Experimental Immunology, 174(1), pp. 109-119.Publisher
WileyJournal
Clinical and Experimental ImmunologyPubMed ID
23607934 (pubmed)Additional Links
https://onlinelibrary.wiley.com/doi/full/10.1111/cei.12118Type
Journal articleLanguage
enDescription
© 2013 The Authors. Published by Wiley. This is an open access article available under a Creative Commons licence. The published version can be accessed at the following link on the publisher’s website: https://doi.org/10.1111/cei.12118ISSN
0009-9104EISSN
1365-2249Sponsors
This work was supported by Marie Curie Intra European Fellowship (FP7‐people‐IEF‐2008‐235993), St Mark's Hospital Foundation the Brigid Balfour Fund and the BBSRC (WMNI P33458).ae974a485f413a2113503eed53cd6c53
10.1111/cei.12118
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Except where otherwise noted, this item's license is described as https://creativecommons.org/licenses/by-nc-nd/4.0/
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