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Effect of nasopharyngeal carcinoma-derived exosomes on human regulatory T cells

JNCI : Journal of the National Cancer Institute, 2015-01, Vol.107 (1), p.363-363 [Peer Reviewed Journal]

The Author 2014. Published by Oxford University Press. All rights reserved. For Permissions, please e-mail: journals.permissions@oup.com. ;Copyright Oxford Publishing Limited(England) Jan 2015 ;Distributed under a Creative Commons Attribution 4.0 International License ;ISSN: 0027-8874 ;EISSN: 1460-2105 ;DOI: 10.1093/jnci/dju363 ;PMID: 25505237 ;CODEN: JNCIEQ

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Title:
Effect of nasopharyngeal carcinoma-derived exosomes on human regulatory T cells
Author: Mrizak, Dhafer ; Martin, Nathalie ; Barjon, Clément ; Jimenez-Pailhes, Anne-Sophie ; Mustapha, Rami ; Niki, Toshiro ; Guigay, Joël ; Pancré, Véronique ; de Launoit, Yvan ; Busson, Pierre ; Moralès, Olivier ; Delhem, Nadira
Subjects: Animals ; Blotting, Western ; Cancer ; Carcinoma - immunology ; Carcinoma - metabolism ; CD4-Positive T-Lymphocytes - immunology ; CD4-Positive T-Lymphocytes - metabolism ; Cell Line, Tumor ; Cell Proliferation ; Chemokine CCL20 - metabolism ; Cytokines ; Exosomes - immunology ; Exosomes - metabolism ; Flow Cytometry ; Forkhead Transcription Factors - metabolism ; Gene Expression Regulation, Neoplastic ; Heterografts ; Humans ; Interleukin-10 - immunology ; Interleukin-2 Receptor alpha Subunit - metabolism ; Life Sciences ; Mice ; Mice, SCID ; Monoclonal antibodies ; Nasopharyngeal Neoplasms - immunology ; Nasopharyngeal Neoplasms - metabolism ; Plasma ; Real-Time Polymerase Chain Reaction ; T cell receptors ; T-Lymphocytes - immunology ; T-Lymphocytes - metabolism ; T-Lymphocytes, Regulatory - immunology ; T-Lymphocytes, Regulatory - metabolism ; Transforming Growth Factor beta1 - immunology ; Tumors
Is Part Of: JNCI : Journal of the National Cancer Institute, 2015-01, Vol.107 (1), p.363-363
Description: Regulatory T cells (Treg) and tumor-exosomes are thought to play a role in preventing the rejection of malignant cells in patients bearing nasopharyngeal carcinoma (NPC). Treg recruitment by exosomes derived from NPC cell lines (C15/C17-Exo), exosomes isolated from NPC patients' plasma (Patient-Exo), and CCL20 were tested in vitro using Boyden chamber assays and in vivo using a xenograft SCID mouse model (n = 5), both in the presence and absence of anti-CCL20 monoclonal antibodies (mAb). Impact of these NPC exosomes (NPC-Exo) on Treg phenotype and function was determined using adapted assays (FACS, Q-PCR, ELISA, and MLR). Experiments were performed in comparison with exosomes derived from plasma of healthy donors (HD-Exo). The Student's t test was used for group comparisons. All statistical tests were two-sided. CCL20 allowed the intratumoral recruitment of human Treg. NPC-Exo also facilitated Treg recruitment (3.30 ± 0.34 fold increase, P < .001), which was statistically significantly inhibited (P < .001) by an anti-CCL20 blocking mAb. NPC-Exo also recruited conventional CD4(+)CD25(-) T cells and mediated their conversion into inhibitory CD4(+)CD25(high) cells. Moreover, NPC-Exo enhanced (P = .0048) the expansion of human Treg, inducing the generation of Tim3(Low) Treg with increased expression of CD25 and FOXP3. Finally, NPC-Exo induced an overexpression of cell markers associated with Treg phenotype, properties and recruitment capacity. For example, GZMB mean fold change was 21.45 ± 1.75 (P < .001). These results were consistent with a stronger suppression of responder cells' proliferation and the secretion of immunosuppressive cytokines (IL10, TGFB1). Interactions between NPC-Exo and Treg represent a newly defined mechanism that may be involved in regulating peripheral tolerance by tumors and in supporting immune evasion in human NPC.
Publisher: United States: Oxford Publishing Limited (England)
Language: English
Identifier: ISSN: 0027-8874
EISSN: 1460-2105
DOI: 10.1093/jnci/dju363
PMID: 25505237
CODEN: JNCIEQ
Source: GFMER Free Medical Journals
MEDLINE
Alma/SFX Local Collection

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Effect of nasopharyngeal carcinoma-derived exosomes on human regulatory T cells

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