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(Journal of Leukocyte Biology. 2001;69:685-690.)
© 2001 by Society for Leukocyte Biology

Analysis of macrophage activation in African trypanosomiasis

Donna M. Paulnock and Susan P. Coller

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-{gamma}, 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-{gamma}. 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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