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    Amastigote surface proteins of Trypanosoma cruzi are targets for CD8+ CTL

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    Authors
    Low, Hoi Pang
    Santos, Maria A. M.
    Wizel, Benjamin
    Tarleton, Rick L.
    UMass Chan Affiliations
    Department of Neurology
    Document Type
    Journal Article
    Publication Date
    1998-02-20
    Keywords
    Animals
    Antigen Presentation
    Cytotoxicity, Immunologic
    Female
    H-2 Antigens
    Membrane Proteins
    Mice
    Mice, Inbred C57BL
    Neuraminidase
    Protein Binding
    Protozoan Proteins
    T-Lymphocytes, Cytotoxic
    Trypanosoma cruzi
    Immunology and Infectious Disease
    Molecular and Cellular Neuroscience
    Neuroscience and Neurobiology
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    Link to Full Text
    http://www.jimmunol.org/cgi/pmidlookup?view=long&pmid=9469442
    Abstract
    Amastigotes of Trypanosoma cruzi express surface proteins that, when released into the host cell cytoplasm, are processed and presented on the surface of infected cells in the context of MHC class I molecules to be recognized by CD8+ CTL. To further understand the role of CTL in T. cruzi infection, we used the available MHC class I peptide binding motifs to identify potential CTL target epitopes in two recently described T. cruzi amastigote surface proteins, ASP-1 and ASP-2. The predicted amino acid sequences of ASP-1 and ASP-2 were screened for H-2b allele-specific class I peptide motifs, and four peptides (PA11, PA12, PA13, and PA14) and six peptides (PA5, PA6, PA7, PA8, PA9, and PA10) were synthesized from ASP-1 and ASP-2, respectively. The majority of the peptides bound to some degree to H-2b class I MHC molecules, and six of 10 of the peptides stimulated spleen cells from T. cruzi-infected mice to lyse target cells sensitized with the homologous peptides. Short term T cell lines specific for three of these peptides also lysed T. cruzi-infected target cells. These results demonstrate that ASP-1 and ASP-2 are targets of in vivo generated CTLs and that this CTL response induced by T. cruzi infection is parasite and peptide specific, MHC restricted, and CD8 dependent.
    Source
    J Immunol. 1998 Feb 15;160(4):1817-23.
    Permanent Link to this Item
    http://hdl.handle.net/20.500.14038/37641
    PubMed ID
    9469442
    Related Resources
    Link to Article in PubMed
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    UMass Chan Faculty and Researcher Publications

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