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14 NKT Cells in Lungs and Their Roles in Th1 Response and Host Defense in Cryptococcal Infection1
*
First Department of Internal Medicine, Faculty of Medicine, University of the Ryukyus, Okinawa, Japan; and
Core Research for Evolutional Science and Technology Project, Department of Molecular Immunology, Graduate School of Medicine, Chiba University, Chiba, Japan
To elucidate the role of NKT cells in the host defense to
cryptococcal infection, we examined the proportion of these cells,
identified by the expression of CD3 and NK1.1, in lungs after
intratracheal infection with Cryptococcus neoformans.
This population increased on day 3 after infection, reached a peak
level on days 6–7, and decreased thereafter. In V
14 NKT
cell-deficient mice, such increase was significantly attenuated. The
proportion of V14 NKT cells, detected by binding to
-galactosylceramide-loaded CD1d tetramer, and the expression of
V14 mRNA increased after infection with a similar kinetics. The
delayed-type hypersensitivity response and differentiation of the
fungus-specific Th1 cells was reduced in V14 NKT cell-deficient
mice, compared with control mice. Additionally, elimination of this
fungal pathogen from lungs was significantly delayed in V14 NKT
cell-deficient mice. Production of monocyte chemoattractant protein
(MCP)-1 in lungs, detected at both mRNA and protein levels,
increased on day 1, reached a peak level on day 3, and decreased
thereafter, which preceded the increase in NKT cells. Finally, the
increase of total and V14+ subset of NKT cells after
infection was significantly reduced in MCP-1-deficient mice. Our
results demonstrated that NKT cells, especially V14+
subset, accumulated in a MCP-1-dependent manner in the lungs after
infection with C. neoformans and played an important
role in the development of Th1 response and host resistance to this
fungal pathogen.
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