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ß T Cells in IL-12 Production During Salmonella Infection1
*
Laboratory of Host Defense and Germfree Life, Research Institute for Disease Mechanism and Control, Nagoya University School of Medicine, Nagoya, Japan;
Core Research for Evolutional Science and Technology (CREST), Japan Science and Technology Corporation, and Division of Molecular Immunology, Center for Biomedical Science, School of Medicine, Chiba University, Chiba, Japan; and
Institute for Physical and Chemical Reseach Brain Science Institute, Saitama, Japan
NK1.1+
ß T cells emerge in the peritoneal cavity
after an i.p. infection with Salmonella choleraesuis in
mice. To elucidate the role of the NK1.1+ß T cells
during murine salmonellosis, mice lacking NK1.1+ß T
cells by disruption of TCRß (TCRß-/-),
ß2m (ß2m-/-), or J281
(J281-/-) gene were i.p. inoculated with S.
choleraesuis. The peritoneal exudate T cells in wild type (wt)
mice on day 3 after infection produced IL-4 upon TCRß stimulation,
whereas those in TCRß-/-,
ß2m-/-, or J281-/- mice
showed no IL-4 production upon the stimulation, indicating that
NK1.1+ß T cells are the main source of IL-4 production
at the early phase of Salmonella infection.
Neutralization of endogenous IL-4 by administration of anti-IL-4
mAb to wt mice reduced the number of Salmonella
accompanied by increased IL-12 production by macrophages after
Salmonella infection. The IL-12 production by the
peritoneal macrophages was significantly augmented in mice lacking
NK1.1+ß T cells after Salmonella
infection accompanied by increased serum IFN-
level. The aberrantly
increased IL-12 production in infected TCRß-/- or
J281-/- mice was suppressed by adoptive transfer of T
cells containing NK1.1+ß T cells but not by the
transfer of T cells depleted of NK1.1+ß T cells or T
cells from J281-/- mice. Taken together, it is
suggested that NK1.1+ß T cells eliciting IL-4 have a
regulatory function in the IL-12 production by macrophages at the early
phase of Salmonella infection.
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