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* World Health Organization Immunology Research and Training Center, Institute of Biochemistry, University of Lausanne, and
Ludwig Institute for Cancer Research, Lausanne Branch, Epalinges, Switzerland
Susceptibility and development of Th2 cells in BALB/c mice infected
with Leishmania major result from early IL-4 production
by V
4V
8 CD4+ T cells in response to the
Leishmania homolog of mammalian RACK1 Ag. A role
for CD4+CD25+ regulatory T cells in the control
of this early IL-4 production was investigated by depleting in vivo
this regulatory T cell population. Depletion induced an increase in the
early burst of IL-4 mRNA in the draining lymph nodes of BALB/c mice,
and exacerbated the course of disease with higher levels of IL-4 mRNA
and protein in their lymph nodes. We further showed that transfer of
107 BALB/c spleen cells that were depleted of
CD4+CD25+ regulatory T cells rendered SCID mice
susceptible to infection and allowed Th2 differentiation while SCID
mice reconstituted with 107 control BALB/c spleen cells
were resistant to infection with L. major and developed
a Th1 response. Treatment with a mAb against IL-4 upon infection with
L. major in SCID mice reconstituted with CD25-depleted
spleen cells prevented the development of Th2 polarization and rendered
them resistant to infection. These results demonstrate that
CD4+CD25+ regulatory T cells play a role in
regulating the early IL-4 mRNA and the subsequent development of a Th2
response in this model of infection.
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