{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,18]],"date-time":"2026-08-18T00:47:04Z","timestamp":1787014024534,"version":"build-2736575974"},"reference-count":46,"publisher":"Wiley","issue":"2","license":[{"start":{"date-parts":[[2014,10,31]],"date-time":"2014-10-31T00:00:00Z","timestamp":1414713600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"},{"start":{"date-parts":[[2014,10,31]],"date-time":"2014-10-31T00:00:00Z","timestamp":1414713600000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"funder":[{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","award":["AI095835"],"award-info":[{"award-number":["AI095835"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","award":["AI103338"],"award-info":[{"award-number":["AI103338"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]},{"name":"NCI","award":["CA013330"],"award-info":[{"award-number":["CA013330"]}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Cellular Microbiology"],"published-print":{"date-parts":[[2015,2]]},"abstract":"Summary<\/jats:title>\n \n Inducing long\u2010term protective memory\n CD<\/jats:styled-content>\n 8\n +<\/jats:sup>\n T<\/jats:styled-content>\n \u2010cells is a desirable goal for vaccines against intracellular pathogens. However, the mechanisms of differentiation of\n CD<\/jats:styled-content>\n 8\n +<\/jats:sup>\n T<\/jats:styled-content>\n \u2010cells into long\u2010lived memory cells capable of mediating protection of immunized hosts remain incompletely understood. We have developed an experimental system using mice immunized with wild type (WT) or mutants of the intracellular bacterium\n Listeria monocytogenes<\/jats:italic>\n (\n \n Lm<\/jats:italic>\n <\/jats:styled-content>\n ) that either do or do not develop protective memory\n CD<\/jats:styled-content>\n 8\n +<\/jats:sup>\n T\u2010cells. We previously reported that mice immunized with\n \n Lm<\/jats:italic>\n <\/jats:styled-content>\n lacking functional\n SecA2<\/jats:styled-content>\n , an auxiliary secretion system of gram\u2010positive bacteria, did not differentiate functional memory\n CD<\/jats:styled-content>\n 8\n +<\/jats:sup>\n T\u2010cells that protected against a challenge infection with\n \n WT\n Lm<\/jats:italic>\n <\/jats:styled-content>\n . Herein we hypothesized that the p60 and\n NamA<\/jats:styled-content>\n autolysins of\n \n Lm<\/jats:italic>\n <\/jats:styled-content>\n , which are major substrates of the\n SecA2<\/jats:styled-content>\n pathway, account for this phenotype. We generated\n \n Lm<\/jats:italic>\n <\/jats:styled-content>\n genetically deficient for genes encoding for the p60 and\n NamA<\/jats:styled-content>\n proteins,\n \n \u0394iap\u0394murA Lm<\/jats:italic>\n <\/jats:styled-content>\n , and further characterized this mutant.\n \n \u0394p60\u0394NamA\n Lm<\/jats:italic>\n <\/jats:styled-content>\n exhibited a strong filamentous phenotype, inefficiently colonized host tissues, and grew mostly outside cells. When\n \n \u0394p60\u0394NamA\n Lm<\/jats:italic>\n <\/jats:styled-content>\n was made single unit, cell invasion was restored to\n WT<\/jats:styled-content>\n levels during vaccination, yet induced memory T\u2010cells still did not protect immunized hosts against recall infection. Recruitment of blood phagocytes and antigen\u2010presenting cell activation was close to that of mice immunized with\n \n \u0394ActA\n Lm<\/jats:italic>\n <\/jats:styled-content>\n , which develop protective memory. However, key inflammatory factors involved in optimal\n T<\/jats:styled-content>\n \u2010cell programming such as\n IL<\/jats:styled-content>\n \u201012 and type\n I IFN<\/jats:styled-content>\n (\n IFN<\/jats:styled-content>\n \u2010\n I<\/jats:styled-content>\n ) were lacking, suggesting that cytokine signals may largely account for the observed phenotype. Thus, altogether, these results establish that p60 and\n NamA<\/jats:styled-content>\n secreted by\n \n Lm<\/jats:italic>\n <\/jats:styled-content>\n promote primary host cell invasion, the inflammatory response and the differentiation of functional memory\n CD<\/jats:styled-content>\n 8\n +<\/jats:sup>\n T\u2010cells, by preventing\n \n Lm<\/jats:italic>\n <\/jats:styled-content>\n filamentation during growth and subsequent triggering of innate sensing mechanisms.\n <\/jats:p>","DOI":"10.1111\/cmi.12362","type":"journal-article","created":{"date-parts":[[2014,9,16]],"date-time":"2014-09-16T06:07:20Z","timestamp":1410847640000},"page":"147-163","source":"Crossref","is-referenced-by-count":12,"title":["The p60 and\n NamA<\/scp>\n autolysins from\n \n L<\/i>\n <\/scp>\n isteria monocytogenes<\/i>\n contribute to host colonization and induction of protective memory"],"prefix":"10.1155","volume":"17","author":[{"given":"Ceena","family":"Chandrabos","sequence":"first","affiliation":[{"name":"Department of Microbiology and Immunology Albert Einstein College of Medicine Bronx NY 10461 USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sa\u00efdi M'Homa","family":"Soudja","sequence":"additional","affiliation":[{"name":"Department of Microbiology and Immunology Albert Einstein College of Medicine Bronx NY 10461 USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Brian","family":"Weinrick","sequence":"additional","affiliation":[{"name":"Department of Microbiology and Immunology Albert Einstein College of Medicine Bronx NY 10461 USA"},{"name":"Howard Hughes Medical Institute, Albert Einstein College of Medicine Bronx NY USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Marilyn","family":"Gros","sequence":"additional","affiliation":[{"name":"Department of Microbiology and Immunology Albert Einstein College of Medicine Bronx NY 10461 USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Aurel","family":"Frangaj","sequence":"additional","affiliation":[{"name":"Department of Microbiology and Immunology Albert Einstein College of Medicine Bronx NY 10461 USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Massilva","family":"Rahmoun","sequence":"additional","affiliation":[{"name":"Institut National de la Sant\u00e9 et de la Recherche M\u00e9dicale U924, Groupe Avenir Institut de Pharmacologie Mol\u00e9culaire et Cellulaire Valbonne 06560 France"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"suffix":"Jr","given":"William R.","family":"Jacobs","sequence":"additional","affiliation":[{"name":"Department of Microbiology and Immunology Albert Einstein College of Medicine Bronx NY 10461 USA"},{"name":"Howard Hughes Medical Institute, Albert Einstein College of Medicine Bronx NY USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Gr\u00e9goire","family":"Lauvau","sequence":"additional","affiliation":[{"name":"Department of Microbiology and Immunology Albert Einstein College of Medicine Bronx NY 10461 USA"},{"name":"Institut National de la Sant\u00e9 et de la Recherche M\u00e9dicale U924, Groupe Avenir Institut de Pharmacologie Mol\u00e9culaire et Cellulaire Valbonne 06560 France"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2014,10,31]]},"reference":[{"key":"e_1_2_8_2_1","doi-asserted-by":"publisher","DOI":"10.1371\/journal.ppat.1003861"},{"key":"e_1_2_8_3_1","doi-asserted-by":"crossref","first-page":"2266","DOI":"10.4049\/jimmunol.138.7.2266","article-title":"Intracellular growth of Listeria monocytogenes as a prerequisite for in vivo induction of T cell\u2010mediated immunity","volume":"138","author":"Berche P.","year":"1987","journal-title":"J 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