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In Vivo1
,
Departments of
*
Pathology,
Microbiology and Immunology, and
Medicine, School of Medicine, University of North Carolina, Chapel Hill, NC 27599; and
§
Department of Internal Medicine, University of Michigan Medical School, Ann Arbor, MI 48109
Chemokines are small proteins that direct the migration of
leukocytes to inflammatory foci. Many cell types, including
macrophages, fibroblasts, endothelial cells, and lymphocytes, produce
chemokines in vitro, but biologically relevant sources of chemokines in
vivo have not been well characterized. To investigate the pertinent
sources of macrophage inflammatory protein-1
(MIP-1) in vivo, we
used MIP-1-deficient (MIP-1-/-) mice as
donors and as recipients in adoptive transfer experiments after a
lethal infection with Listeria monocytogenes (LM).
Unexpectedly, we found that the production of MIP-1 by
CD8+ T cells was critical in this system, as the cells from
MIP-1-/- mice primed with LM were significantly less
effective in protecting naive mice against a lethal infection by LM
than were the CD8+ T cells from wild-type (wt) mice.
This requirement for donor T cell production of MIP-1 was confirmed
by the observation that wt donor T cells do not mediate protection when
coadministered with an anti-MIP-1 polyclonal antiserum.
Production of MIP-1 by the recipient mice was not required for
protection, because wt and MIP-1-/- recipients were
equally well protected by wt T cells. A 2- to 3-fold decrease in the
number of transferred lymphocytes was seen in the spleens of mice
receiving T cells from MIP-1-/- mice compared with
those receiving wt T cells. In addition, CD8+ T cells from
MIP-1-/- mice had a reduced ability to kill
LM-infected target cells in vitro. These findings demonstrate that T
cell production of MIP-1 is required for clearance of an
intracellular pathogen in vivo.
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