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Unité de Biologie Moléculaire du Gène, Institut National de la Santé et de la Recherche Médicale, Unité 277, Département d’Immunologie, Institut Pasteur, Paris, France;
Institut de Pharmacologie et de Biologie Structurale du Centre National de la Recherche Scientifique, Toulouse, France;
Howard Hughes Medical Institute, Department of Microbiology and Immunology, Vanderbilt University School of Medicine, Nashville, TN; and
Institut National de la Santé et de la Recherche Médicale, Unité 25, Hôpital Necker, Paris, France
Murine V
14invT cells (NKT cells), restricted by the
CD1d1 MHC 1b molecules, are a distinctive subset of T cells endowed
with pleiotropic functions. CD1d1-restricted NKT cells infiltrate the
granulomas induced by the s.c. injection of mycobacterial
phosphatidylinositoldimannoside (PIM2) but not of its
deacylated derivative. NKT cells are detectable as early as 6 hours
following the injection. Although the molecular structure of
PIM2 meets the requirements for presentation by CD1d1, Ab
blocking and adoptive transfer experiments of wild-type NKT cells into
CD1d1-/- mice show that CD1d1 expression is not required
for the early recruitment of NKT cells to the injection site. This
conclusion was confirmed by the finding that IL-12R
-/-
and CD40-/- mice were able to recruit NKT cells after
PIM2 challenge. Moreover, the injection of
-galactosylceramide, an NKT cell ligand that is recognized in the
context of CD1d1, promoted only a minor recruitment of NKT cells. By
contrast, injection of -galactosylceramide, a synthetic glycolipid
that binds to CD1d1 but does not activate the CD1d/TCR pathway,
resulted in the development of large granulomas rich in NKT cells.
Finally, local injection of TNF- mimics the effect of glycolipids.
It is concluded that NKT cells migrate to and accumulate at
inflammatory sites in the same way as other cells of the innate immune
system and that migration to and accumulation at inflammatory sites are
processes independent of the CD1d1 molecule.
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