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* Department of Pathology and Laboratory Medicine, University of Wisconsin Medical School, and
Department of Pathobiological Sciences, School of Veterinary Medicine, University of Wisconsin, Madison, WI 53706; and
Department of Internal Medicine, University of Iowa, Iowa City, IA 52242
The hallmark of Schistosoma mansoni infection is the
formation of liver granulomas around deposited ova. The initiation of
granuloma formation is T cell-dependent since granulomas are not formed
in their absence. We investigated whether a few T cells arrive to
initiate the inflammatory lesion and subsequently expand locally, or
whether a large repertoire of systemically activated T cells home to
the delayed type hypersensitivity reaction induced by the ova. The TCR
repertoire of single granulomas from the same liver were analyzed by
PCR using V
-specific primers and CDR3 analysis. Each granuloma has a
very diverse TCR repertoire indicating that most of the T cells
recruited to these lesions are activated systemically. At the same
time, sequence analysis of individually sized CDR3 products from single
granuloma indicate that a fraction of T cells expand locally at the
lesion site. Using TCR transgenic mice containing a pigeon cytochrome
c-specific T cell population or lymphocytic
choriomeningitis virus infection tracked with lymphocytic
choriomeningitis virus-specific tetramers, we demonstrated that
nonspecific T cells home to the granuloma if they are activated.
However, recombinase-activating gene 2-/- pigeon
cytochrome c-specific TCR transgenic mice fail to
form granulomas in response to S. mansoni ova even after
T cell activation, suggesting a requirement for egg-specific T cells in
the initiation of these inflammatory lesions. Understanding the
mechanism of T cell recruitment into granulomas has important
implications for the rational design of immunotherapies for
granulomatous diseases.
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