{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,6]],"date-time":"2026-10-06T14:02:20Z","timestamp":1791295340921,"version":"4.1.0"},"reference-count":53,"publisher":"American Society for Microbiology","issue":"5","license":[{"start":{"date-parts":[[2011,5,1]],"date-time":"2011-05-01T00:00:00Z","timestamp":1304208000000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.asm.org\/non-commercial-tdm-license"}],"content-domain":{"domain":["journals.asm.org"],"crossmark-restriction":true},"short-container-title":["Infect Immun"],"published-print":{"date-parts":[[2011,5]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n          <jats:p>\n            CD8\n            <jats:sup>+<\/jats:sup>\n            T lymphocytes often play a primary role in adaptive immunity to cytosolic microbial pathogens. Surprisingly, CD8\n            <jats:sup>+<\/jats:sup>\n            T cells are not required for protective immunity to the enteric pathogen\n            <jats:named-content xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" content-type=\"genus-species\" xlink:type=\"simple\">Shigella flexneri<\/jats:named-content>\n            , despite the ability of\n            <jats:named-content xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" content-type=\"genus-species\" xlink:type=\"simple\">Shigella<\/jats:named-content>\n            to actively secrete proteins into the host cytoplasm, a location from which antigenic peptides are processed for presentation to CD8\n            <jats:sup>+<\/jats:sup>\n            T cells. To determine why CD8\n            <jats:sup>+<\/jats:sup>\n            T cells fail to play a role in adaptive immunity to\n            <jats:named-content xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" content-type=\"genus-species\" xlink:type=\"simple\">S. flexneri<\/jats:named-content>\n            , we investigated whether antigen-specific CD8\n            <jats:sup>+<\/jats:sup>\n            T cells are primed during infection but are unable to confer protection or, alternatively, whether T cells fail to be primed. To test whether\n            <jats:named-content xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" content-type=\"genus-species\" xlink:type=\"simple\">Shigella<\/jats:named-content>\n            is capable of stimulating an antigen-specific CD8\n            <jats:sup>+<\/jats:sup>\n            T-cell response, we created an\n            <jats:named-content xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" content-type=\"genus-species\" xlink:type=\"simple\">S. flexneri<\/jats:named-content>\n            strain that constitutively secretes a viral CD8\n            <jats:sup>+<\/jats:sup>\n            T-cell epitope via the\n            <jats:named-content xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" content-type=\"genus-species\" xlink:type=\"simple\">Shigella<\/jats:named-content>\n            type III secretion system and characterized the CD8\n            <jats:sup>+<\/jats:sup>\n            T-cell response to this strain both in mice and in cultured cells. Surprisingly, no T cells specific for the viral epitope were stimulated in mice infected with this strain, and cells infected with the recombinant strain were not targeted by epitope-specific T cells. Additionally, we found that the usually robust T-cell response to antigens artificially introduced into the cytoplasm of cultured cells was significantly reduced when the antigen-presenting cell was infected with\n            <jats:named-content xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" content-type=\"genus-species\" xlink:type=\"simple\">Shigella<\/jats:named-content>\n            . Collectively, these results suggest that antigen-specific CD8\n            <jats:sup>+<\/jats:sup>\n            T cells are not primed during\n            <jats:named-content xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" content-type=\"genus-species\" xlink:type=\"simple\">S. flexneri<\/jats:named-content>\n            infection and, as a result, afford little protection to the host during primary or subsequent infection.\n          <\/jats:p>","DOI":"10.1128\/iai.00939-10","type":"journal-article","created":{"date-parts":[[2011,3,1]],"date-time":"2011-03-01T21:45:09Z","timestamp":1299015909000},"page":"2021-2030","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":19,"title":["Antigen-Specific CD8\n            <sup>+<\/sup>\n            T Cells Fail To Respond to Shigella flexneri"],"prefix":"10.1128","volume":"79","author":[{"given":"Stephanie P.","family":"Jehl","sequence":"first","affiliation":[{"name":"Department of Microbiology and Molecular Genetics, Harvard Medical School, Boston, Massachusetts 02115"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Amy M.","family":"Doling","sequence":"additional","affiliation":[{"name":"Department of Microbiology and Molecular Genetics, Harvard Medical School, Boston, Massachusetts 02115"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kara S.","family":"Giddings","sequence":"additional","affiliation":[{"name":"Department of Microbiology and Molecular Genetics, Harvard Medical School, Boston, Massachusetts 02115"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Armelle","family":"Phalipon","sequence":"additional","affiliation":[{"name":"Unit\u00e9 de Pathog\u00e9nie Microbienne Mol\u00e9culaire, INSERM U786, Institut Pasteur, 75724 Paris Cedex 15, France"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Philippe J.","family":"Sansonetti","sequence":"additional","affiliation":[{"name":"Unit\u00e9 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