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HTLV-1 propels thymic human T cell development in "human immune system" Rag2-/- IL-2R γc-/- Mice

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HAL Id: inserm-00663648

https://www.hal.inserm.fr/inserm-00663648

Submitted on 27 Jan 2012

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HTLV-1 propels thymic human T cell development in

”human immune system” Rag2-/- IL-2R γc-/- Mice

Julien Villaudy, Melanie Wencker, Nicolas Gadot, Jean-Yves Scoazec, Louis

Gazzolo, Markus Manz, Madeleine Duc Dodon

To cite this version:

Julien Villaudy, Melanie Wencker, Nicolas Gadot, Jean-Yves Scoazec, Louis Gazzolo, et al.. HTLV-1

propels thymic human T cell development in ”human immune system” Rag2-/- IL-2R γc-/- Mice.

15th International Conference on Human Retroviruses: HTLV and Related Viruses, Jun 2011, Leuven

and Gembloux, Belgium. pp.A10, �10.1186/1742-4690-8-S1-A10�. �inserm-00663648�

(2)

MEETING ABSTRACT

Open Access

HTLV-1 propels thymic human T cell

development in

“human immune system”

Rag2-/-IL-2R

gc-/- Mice

Julien Villaudy

1

, Melanie Wencker

1

, Nicolas Gadot

2

, Jean-Yves Scoazec

2

, Louis Gazzolo

1

, Markus G Manz

3,4

,

Madeleine Duc Dodon

1*

From 15th International Conference on Human Retroviruses: HTLV and Related Viruses

Leuven and Gembloux, Belgium. 5-8 June 2011

Alteration of early haematopoietic development is thought to be responsible for the onset of immature leu-kemias and lymphomas. We have previously shown that HTLV-1 (Human T cell Leukemia Virus type 1) is able not only to infect immature thymocytes in vitro but also, through Tax expression, to alter the b-selection checkpoint critical for early T cell development. To further clarify the role of the natural HTLV-1 infection on human T-cell development, we developed an in vivo model by transplanting immunocompromised Rag2-/-gc-/- newborn mice with human cord blood CD34+ cells to obtain Human Immune System (HIS) mice. In these mice the development of human T cells in the thymus is fully developed within two months after human cell transplantation. Lethally irradiated HTLV-1 producing cells were then injected into these HIS mice. Herein we observed in the thymus of the infected ani-mals an enlarged population of mature T cells when compared with the mock-infected mice. Furthermore, we noted an increased number of CD4+ cells expressing CD25. Infected animals also developed, several weeks after the infection, pathological features such as spleno-megaly, adenopathy, thymomas, lymphomas and leuke-mias in which predominate human T cells, with a large proportion of CD25+ activated cells. Tax expression especially in the lymphomas and thymomas correlated with an up-regulation of NF-B regulated genes. Alto-gether, these results underline that this HIS Rag2-/-gc-/-model might be of great interest to study the

leukemogenic process induced by HTLV-1 as well as to validate new therapeutic approaches of ATL.

Author details

1

Virologie Humaine, INSERM-U758, Ecole Normale Supérieure de Lyon, IFR 128 BioSciences Lyon-Gerland, Lyon, 69364, Cedex 07, France.2Anipath, UFR

Médecine Lyon-RTH Laennec, Lyon, 69372, Cedex 08, France.3Institute for

research in Biomedicine (IRB), Bellinzona, 6500, Switzerland.4Division of

Hematology, University and University Hospital Zürich, Zürich, 8091, Switzerland.

Published: 6 June 2011

doi:10.1186/1742-4690-8-S1-A10

Cite this article as: Villaudy et al.: HTLV-1 propels thymic human T cell development in“human immune system” Rag2-/- IL-2R gc-/- Mice. Retrovirology 2011 8(Suppl 1):A10.

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* Correspondence: mducdodo@ens-lyon.fr

1

Virologie Humaine, INSERM-U758, Ecole Normale Supérieure de Lyon, IFR 128 BioSciences Lyon-Gerland, Lyon, 69364, Cedex 07, France

Full list of author information is available at the end of the article Villaudy et al. Retrovirology 2011,8(Suppl 1):A10

http://www.retrovirology.com/content/8/S1/A10

© 2011 Villaudy 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.

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