Department of Medical Microbiology and Immunology, University of Wisconsin Medical School, Madison, Wisconsin
Correspondence: Donna M. Paulnock, Ph.D., Department of Medical Microbiology and Immunology, University of Wisconsin Medical School, 1300 University Avenue, Madison, WI 53706-1532. E-mail: paulnock{at}facstaff.wisc.edu
African trypanosomes cause a fatal disease of man and animals that is
characterized by extensive functional, histological, and pathological
changes in the lymphoid tissues of infected hosts, including an
increase in the numbers and activation state of macrophages. Macrophage
activation during infection is the result of exposure of these cells to
parasite components and host-derived IFN-
, produced in response to
parasite antigens. The balance of these different activation signals
may determine the outcome of infection. In the experiments described
here, we assessed the ability of the variant surface glycoprotein (VSG)
of the organism Trypanosoma brucei rhodesiense (T.b.
rhodesiense) to activate macrophages directly. Our results
demonstrate that macrophages bind and are activated by the VSG
molecule. The resulting profile of activation differs from that
stimulated by IFN-. These results suggest that the interaction of
host macrophages with VSG released during parasite infection may be a
key component of trypanosomiasis.
Key Words: host defense • innate immunity • trypanosomes • gene expression • variant surface glycoprotein
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