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9V
2 T Cells Impair Intracellular Multiplication of Brucella suis in Autologous Monocytes Through Soluble Factor Release and Contact-Dependent Cytotoxic Effect1
Institut National de la Santé et de la Recherche Médicale Unité 431, Microbiologie et Pathologie Cellulaire Infectieuse, Université de Montpellier II, Montpellier, France
Human V
9V
2 T cells are considered to play an important role
in brucellosis, as this population is dramatically increased in
peripheral blood of patients during the acute phase of the infection.
This T lymphocyte population has been largely demonstrated to be
activated by small m.w. nonpeptidic molecules from natural or synthetic
origin. We recently identified a nonpeptidic fraction of
Brucella suis that specifically activates human
V9V2 T cells. Using a two-separate-chambers system, we showed
that Brucella fraction, as well as isopentenyl
pyrophosphate-activated V9V2 T cells, impaired the multiplication
of B. suis in differentiated THP-1 cells through TNF-
and IFN- release. In the present study, using circulating V9V2
T cells and autologous monocytes infected with B. suis,
we provide evidence that 1) intramonocytic multiplication of B.
suis is impaired by supernatants of activated V9V2 T
cells in part via TNF- and IFN-, this impairment occurring
without host cell lysis; 2) unstimulated V9V2 T cells can impair
intracellular bacterial multiplication after their activation by
soluble factors released by infected monocytes; and 3) activated
V9V2 T cells lyse Brucella-infected monocytes in a
contact-dependent manner. Taken together, these results provide
evidence that V9V2 T cells, in addition to being directly
activated by soluble nonpeptidic molecules, can be stimulated to become
highly cytotoxic in the specific presence of infected monocytes;
moreover, they suggest how V9V2 T cells could be triggered and
respond as antibacterial effector cells in the early stages of
Brucella infection.
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