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Blood, 15 August 2008, Vol. 112, No. 4, pp. 1317-1324.
Prepublished online as a Blood First Edition Paper on June 6, 2008; DOI 10.1182/blood-2008-01-136713.
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Submitted January 29, 2008
Accepted May 27, 2008
Long term expansion of effector/memory V 2neg  T cells is a specific blood signature of CMV infection
Vincent Pitard, David Roumanes, Xavier Lafarge, Lionel Couzi, Isabelle Garrigue, Marie-Edith Lafon, Pierre Merville, Jean-Francois Moreau, and Julie Dechanet-Merville*
Universite Bordeaux 2, Bordeaux, France
CNRS UMR 5164, Universite Bordeaux 2, Bordeaux, France
Departement de Nephrologie et Transplantation Renale, CHU Bordeaux, Bordeaux, France
Laboratoire de Virologie, CHU Bordeaux, Bordeaux, France
Laboratoire d'Immunologie, CHU Bordeaux, France, France
* Corresponding author; email: julie.dechanet{at}u-bordeaux2.fr.
The ability of human  T cells to develop immunological memory is still a matter of debate. We have previously demonstrated the involvement of V 2neg  T lymphocytes in the response of immunosuppressed organ recipients to CMV. Herein, we demonstrate their ability to mount an adaptive immune response to CMV in immunocompetent subjects. V 2neg  T cell peripheral blood numbers, repertoire restriction and cytotoxicity against CMV-infected fibroblasts were markedly increased in CMV-seropositive, in comparison to CMV-seronegative, healthy individuals. While V 2neg  T cells were found as naive cells in CMV- individuals, they virtually all exhibited the cytotoxic effector/memory phenotype in CMV+ individuals which is also observed in transplant patients challenged with CMV. This long-term complete remodeling of the V 2neg  T cell population by CMV predicts their ability to exhibit an adaptive anti-CMV response. Consistent with this, we observed that the secondary response to CMV was associated with a faster  T cell expansion and a better resolution of infection than the primary response. In conclusion, the increased level of effector-memory V 2neg  T cells in the peripheral blood is a specific signature of an adaptive immune response to CMV infection of both immunocompetent and immunosuppressed individuals.

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