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Cutting Edge |


* Department of Immunology, Institute for Medical Microbiology and Hygiene, University of Freiburg, Freiburg, Germany; and
Department of Nephrology, University of Kiel, Kiel, Germany
It has been proposed that expression of the chemokine receptor
CCR7 represents a defining factor for nonpolarized central
(CCR7+) and polarized effector memory (CCR7-)
T cells. In this study, we have tested this hypothesis using in
vivo-activated T cells from P14 and SMARTA TCR-transgenic (tg)
mice specific for MHC class I- and II-restricted epitopes of the
lymphocytic choriomeningitis virus (LCMV) glycoprotein. CCR7 cell
surface expression on TCR-tg cells was monitored with a CC chemokine
ligand 19-Ig fusion protein. CC chemokine ligand 19-Ig staining
separated TCR-tg cells activated by LCMV infection into
CCR7- and CCR7+ effector/memory T cell
populations. Nonetheless, both T cell populations isolated from spleen
and liver produced identical amounts of IFN-
after short-term Ag
stimulation. Furthermore, CCR7+ and CCR7- CD8
TCR-tg cells from LCMV-infected mice exhibited similar lytic activity
against LCMV peptide-coated target cells. These results question the
proposed concept of differential effector cell function of
CCR7+ and CCR7- memory T
cells.
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