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 Blood, 1 May 2007, Vol. 109, No. 9, pp. 3649-3657.
Prepublished online as a Blood First Edition Paper on December 29, 2006; DOI 10.1182/blood-2006-01-035717.

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Submitted January 9, 2006
Accepted December 14, 2006

Trapping and apoptosis of novel subsets of memory T lymphocytes expressing CCR6 in the spleen of HIV- infected patients

Cedric Lecureuil, Behazine Combadiere, Elodie Mazoyer, Olivia Bonduelle, Assia Samri, Brigitte Autran, Patrice Debre, and Christophe Combadiere*

INSERM U543, AP-HP, Universite Pierre et Marie Curie-Paris6, Faculte de Medecine, Paris, France

* Corresponding author; email: combad{at}ccr.jussieu.fr.

CCR6, a homeostatic chemokine receptor, is shown here to characterize subsets of both central and effector memory T cells that secrete high levels of IL-2 and TNF-{alpha} in response to polyclonal and antigen-specific stimulation. CCR6+ T lymphocytes disappeared dramatically from the peripheral blood of HIV-infected patients as HIV disease progressed. The capacity of CD4+CCR6+ to secrete multiple cytokines remained intact among HIV-infected long-term non-progressors but was partially lost from subjects with standard disease progression. CCR6+ T lymphocytes, regardless of their CCR7 expression, accumulated in the spleen of HIV-infected patients, where they died by apoptosis. Assessment of CCR6 expression allowed us to describe novel memory T cell subpopulations capable of high cytokine production and provided evidence of a pathological CCR6-dependent pathway of memory T cell homing that may participate in the loss of memory response against infections.


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