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*
Department of Microbiology and Immunology, University of Maryland, School of Medicine, Baltimore, MD 21201; and
Malaria Program, Naval Medical Research Center, Silver Spring, MD 20910
The liver stage of malaria, caused by the genus
Plasmodium, is clinically silent, but immunologically
significant. Ample evidence exists for an effective CD8+ T
cell response to this stage as well as the involvement of 
T cells
and NK1.1int cells in immunized animal models. In contrast,
there is little information concerning responses in a naive host. Here
we report that several host gene expressions in the liver, spleen, and
kidney of BALB/c mice are altered during the liver stage of
Plasmodium yoelii infection. Really interesting new gene
3 (Ring3), semaphorin subclass 4 member G, glutamylcysteine synthetase,
and p45 NF erythroid 2 were all up-regulated 24 h after infection
with P. yoelii. Semaphorin subclass 4 member G
expression was elevated in the kidney, whereas Ring3 was elevated in
both spleen and kidney. The expression of TNF-
(TNF- and IFN-)
were down-regulated in all three tissues tested except in infected
spleen where IFN- was elevated. P. yoelii-related
host gene changes were compared with those in Toxoplasma
gondii-infected livers. Ring3 expression increased 5-fold over
control values, whereas expression of the other transcripts remained
unchanged. TNF- and IFN- expressions were increased in the
Toxoplasma-infected livers. The uniform increase of
Ring3 expression in both Plasmodium- and
Toxoplasma-infected livers suggests an innate immune
response against parasitic infections, whereas the other gene
expression changes are consistent with Plasmodium
parasite-specific responses. Taken together, these changes suggest the
immune responses to P. yoelii infection are both
parasite and organ specific.
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