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*
Department of Immunology and Infectious Diseases, and
Cardiovascular Biology Laboratory, Harvard School of Public Health, Boston, MA 02115
The cutaneous growth of Leishmania mexicana was
measured in STAT6-deficient mice
(STAT6-/-) and compared with that in
similarly infected wild-type (STAT6+/+)
mice. Following s.c. inoculation with 5 x 106
amastigotes of L. mexicana into the shaven rump,
STAT6+/+ mice developed large, nonhealing
cutaneous lesions, while STAT6-/- mice
failed to develop detectable lesions during most of the course of
study. As infection progressed, STAT6+/+
mice infected with L. mexicana displayed significantly
higher titers of Leishmania-specific IgG1 and IgE
compared with STAT6-/- mice, which
conversely produced significantly higher titers of
Leishmania-specific IgG2a, indicating development of a
Th1-like response in the latter group. At 12 wk postinfection,
Leishmania Ag-stimulated lymph node cells from
STAT6-/- mice produced significantly
higher amounts of IL-12 and IFN-
than those from
STAT6+/+ mice as measured by ELISA. However,
there was no significant difference in IL-4 production between the two
groups. Semiquantitative RT-PCR of transcript levels in intact draining
lymph nodes and skin from inoculation sites confirmed a similar pattern
of cytokines in vivo as that observed in stimulated lymph node cells in
vitro. These results indicate that STAT6-mediated IL-4 signaling is
critical for progression of L. mexicana infection in
genetically susceptible mice and demonstrate that in the absence of
STAT6, susceptible mice default toward a Th1-like response and control
cutaneous L. mexicana infection.
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