• Aucun résultat trouvé

Distinct DC subsets are not equally susceptible to HTLV-1 infection

N/A
N/A
Protected

Academic year: 2021

Partager "Distinct DC subsets are not equally susceptible to HTLV-1 infection"

Copied!
2
0
0

Texte intégral

(1)

HAL Id: inserm-00924953

https://www.hal.inserm.fr/inserm-00924953

Submitted on 7 Jan 2014

HAL is a multi-disciplinary open access

archive for the deposit and dissemination of

sci-entific research documents, whether they are

pub-lished or not. The documents may come from

teaching and research institutions in France or

abroad, or from public or private research centers.

L’archive ouverte pluridisciplinaire HAL, est

destinée au dépôt et à la diffusion de documents

scientifiques de niveau recherche, publiés ou non,

émanant des établissements d’enseignement et de

recherche français ou étrangers, des laboratoires

publics ou privés.

Distinct DC subsets are not equally susceptible to

HTLV-1 infection

Sandrine Alais, Audrey Glaize, Anne Cachat, Florian Lamouche, Renaud

Mahieux, Hélène Dutartre

To cite this version:

Sandrine Alais, Audrey Glaize, Anne Cachat, Florian Lamouche, Renaud Mahieux, et al.. Distinct

DC subsets are not equally susceptible to HTLV-1 infection. 16th International Conference on Human

Retroviruses: HTLV and Related Viruses, Jun 2013, Montreal, Canada. pp.O20,

�10.1186/1742-4690-11-S1-O20�. �inserm-00924953�

(2)

O R A L P R E S E N T A T I O N

Open Access

Distinct DC subsets are not equally susceptible to

HTLV-1 infection

Sandrine Alais, Audrey Glaize, Anne Cachat, Florian Lamouche, Renaud Mahieux, Hélène Dutartre

*

From

16th International Conference on Human Retroviruses: HTLV and Related Viruses

Montreal, Canada. 26-30 June 2013

Beside lymphocytes, HTLV-1 can infect monocytes, blood-or monocytes-derived dendritic cells (DCs) and plasmacy-toïd DCs in vitro. Considering that DCs might be the first cells to be infected during primo infection, we hypothesize that they may constitute viral reservoirs and eventually spread the virus to surrounding lymphocytes. Interestingly, ATL and HAM/TSP diseases display opposite immunolo-gical features, i.e. an impaired CTL response versus a chronic inflammation respectively. Since DCs are major effectors of both innate and adaptative immune responses, infection of specific DC subsets and the subsequent altera-tion of their funcaltera-tions might also lead to the orientaaltera-tion of the adaptive immune response towards either viral toler-ance associated with impaired CTL responses or chronic inflammation, and thus directly participate to the determi-nation of the infection outcome. Using various cytokines cocktails, we therefore generated distinct monocytes-derived DC (MDDC) subsets and infected these cells with HTLV-1 biofilm. We first show that the different MDDC subsets are not equally susceptible to HTLV-1 infection, as measured by FACS analyses and real time PCR assays. We then show that following infection, DC activation or IFN alpha production are not affected by infection in the MDDC subtypes tested. However, while DC maturation alters their susceptibility to the virus, we demonstrate that IFN alpha treatment does not. Finally, the ability of MDDC subsets to transmit HTLV-1 to T-cells will be dis-cussed. Taken together, our results suggest that differential susceptibility of various DC subsets to HTLV-1 infection could differently shape immune responses and therefore affect viral pathogenesis.

Published: 7 January 2014

doi:10.1186/1742-4690-11-S1-O20

Cite this article as:Alais et al.: Distinct DC subsets are not equally susceptible to HTLV-1 infection. Retrovirology 2014 11(Suppl 1):O20.

Submit your next manuscript to BioMed Central and take full advantage of:

• Convenient online submission

• Thorough peer review

• No space constraints or color figure charges

• Immediate publication on acceptance

• Inclusion in PubMed, CAS, Scopus and Google Scholar

• Research which is freely available for redistribution

Submit your manuscript at www.biomedcentral.com/submit

* Correspondence: helene.dutartre@ens-lyon.fr

Oncogenèse Rétrovirale, label Ligue Nationale Contre le Cancer, CIRI, Labex Ecofect, INSERM U1111-CNRS UMR5308, Ecole Normale Supérieure, Université Lyon 1 (UCLB) Lyon, Cedex 07, France

Alais et al. Retrovirology 2014, 11(Suppl 1):O20 http://www.retrovirology.com/content/11/S1/O20

© 2014 Alais et al; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. The Creative Commons Public Domain Dedication waiver (http:// creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

Références

Documents relatifs

Table 1 Differential expression of genes involved in the human antiviral response in unsorted cultures (Uns-C), enriched neurons (En-N), and enriched astrocytes (En-As)...

The primary chicken aortic endothelial cells (pchAEC) were used to assess, for the fi rst time, (i) the innate immune responses of chicken EC stimulated with various

Jouer avec les mots N’est pas de tout repos Car même les plus sots Ont aussi leur défaut Avec un point il le faut. Je mets fin à tous

In bacterial infections, according to the infected tissue and the nature of pathogens, the body responds by mobilizing various actors. I decided to use zebrafish

Higher peripheral CD14 − monocyte counts at 14 days prior to expected calving date associated with a decreased risk of postpartum disease <14 days post‑calving (decreased

In particular, vascular endothelial cells expressed virus antigen in the following tissues: sheath arterioles of spleen of H5N2 virus inoculated Japanese quail; comb of H5N8

Significant KEGG terms related to viral infections and immune signalling were identified through KEGG enrich- ment analyses performed for each up- and down-regu- lated genes (343

Similarly, a high percentage of CD4 + T cells positive for GrB