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Department of Pediatrics and Pathobiology, University of Washington, Seattle, WA 98195
Trypanosoma cruzi is an obligate intracellular
parasite that chronically infects mammals. Extracellular mammalian
stage trypomastigotes simultaneously express and release multiple
members of the parasite’s surface protein superfamily; these
extracellular proteins should stimulate MHC class II-restricted CD4 T
cells. The surface protein superfamily, however, encodes variant
epitopes that may inhibit this CD4 response. In this report the surface
protein-specific CD4 response was investigated. CD4 cells isolated from
acutely and chronically infected mice did not proliferate when
stimulated with surface proteins. Adoptive transfer of surface
protein-specific CD4 clones or immunization with a peptide encoding a
surface protein T cell epitope protected mice during T.
cruzi infection. These data strongly suggested that surface
proteins were expressed and presented to CD4 cells during infection.
Limiting dilution analysis identified an expanded population of surface
protein-specific CD4 cells during the acute and chronic infection.
These surface protein-specific CD4 cells did not produce IL-2 or IL-4,
but did produce IFN-
. Enzyme-linked immunospot analyses confirmed
that many of the surface protein-specific CD4 cells produce IFN-.
Together these results suggest that during T. cruzi
infection a potentially protective CD4 response becomes anergic. It is
possible that this anergy is induced by variant T cell epitopes encoded
by the surface protein superfamily.
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