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Institut für Klinische Mikrobiologie, Immunologie, und Hygiene and
Nachwuchsgruppe 1 des Interdisziplinären Zentrums für Klinische Forschung, Universität Erlangen-Nürnberg, Erlangen, Germany
The resolution of infections with the protozoan parasite
Leishmania major in mice requires a Th1 response that is
closely associated with the expression of IL-12, IFN-
, and inducible
NO synthase. Previous Ab neutralization studies or the use of mice
deficient for both TNF receptors suggested that TNF plays only a
limited role in the control of parasite replication in vivo. In this
study we demonstrate that resistant C57BL/6 (B6.WT) mice
locally infected with L. major rapidly succumb to
progressive visceral leishmaniasis after deletion of the TNF gene by
homologous recombination. A reduction of the parasite inoculum to 3000
promastigotes did not prevent the fatal outcome of the disease. An
influence of the altered morphology of secondary lymphoid organs in
C57BL/6-TNF-/- (B6.TNF-/-) mice on the
course of disease could be excluded by the generation of reciprocal
bone marrow chimeras. Although infected B6.TNF-/- mice
mounted an L. major-specific IFN- response and
expressed IL-12, the onset of the immune reaction was delayed. After in
vitro stimulation, B6.TNF-/- inflammatory macrophages
released 10-fold less NO in response to IFN- than B6.WT cells.
However, in the presence of a costimulus, e.g., L. major
infection or LPS, the production of NO by B6.WT and
B6.TNF-/- macrophages was comparable. In vivo, inducible
NO synthase protein was readily detectable in skin lesions and draining
lymph nodes of B6.TNF-/- mice, but its expression was
more disperse and less focal in the absence of TNF. These are the first
data to demonstrate that TNF is essential for the in vivo control of
L. major.
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