{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,12,31]],"date-time":"2025-12-31T06:57:18Z","timestamp":1767164238890,"version":"build-2238731810"},"reference-count":44,"publisher":"American Society for Microbiology","issue":"2","license":[{"start":{"date-parts":[[2006,2,1]],"date-time":"2006-02-01T00:00:00Z","timestamp":1138752000000},"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":[[2006,2]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:p>\n                    Although \u03b3\u03b4 T cells are a common feature of many pathogen-induced immune responses, the factors that influence, promote, or regulate the response of individual \u03b3\u03b4 T-cell subsets to infection is unknown. Here we show that in the absence of V\u03b31\n                    <jats:sup>+<\/jats:sup>\n                    T cells, novel subsets of \u03b3\u03b4 T cells, expressing T-cell receptor (TCR)-V\u03b3 chains that normally define TCR\u03b3\u03b4\n                    <jats:sup>+<\/jats:sup>\n                    dendritic epidermal T cells (DETCs) (V\u03b35\n                    <jats:sup>+<\/jats:sup>\n                    ), intestinal intraepithelial lymphocytes (iIELs) (V\u03b37\n                    <jats:sup>+<\/jats:sup>\n                    ), and lymphocytes associated with the vaginal epithelia (V\u03b36\n                    <jats:sup>+<\/jats:sup>\n                    ), are recruited to the spleen in response to bacterial infection in TCR-V\u03b31\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    mice. By comparison of phenotype and structure of TCR-V\u03b3 chains and\/or -V\u03b4 chains expressed by these novel subsets with those of their epithelium-associated counterparts, the V\u03b36\n                    <jats:sup>+<\/jats:sup>\n                    T cells elicited in infected V\u03b31\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    mice were shown to be identical to those found in the reproductive tract, from where they are presumably recruited in the absence of V\u03b31\n                    <jats:sup>+<\/jats:sup>\n                    T cells. By contrast, V\u03b35\n                    <jats:sup>+<\/jats:sup>\n                    and V\u03b37\n                    <jats:sup>+<\/jats:sup>\n                    T cells found in infected V\u03b31\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    mice were distinct from V\u03b35\n                    <jats:sup>+<\/jats:sup>\n                    DETCs and V\u03b37\n                    <jats:sup>+<\/jats:sup>\n                    iIELs. Functional analyses of the novel \u03b3\u03b4 T-cell subsets identified for infected V\u03b31\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    mice showed that whereas the V\u03b35\n                    <jats:sup>+<\/jats:sup>\n                    and V\u03b37\n                    <jats:sup>+<\/jats:sup>\n                    subsets may compensate for the absence of V\u03b31\n                    <jats:sup>+<\/jats:sup>\n                    T cells by producing similar cytokines, they do not possess cytocidal activity and they cannot replace the macrophage homeostasis function of V\u03b31\n                    <jats:sup>+<\/jats:sup>\n                    T cells. Collectively, these findings identify novel subsets of \u03b3\u03b4 T cells, the recruitment and activity of which is under the control of V\u03b31\n                    <jats:sup>+<\/jats:sup>\n                    T cells.\n                  <\/jats:p>","DOI":"10.1128\/iai.74.2.1097-1105.2006","type":"journal-article","created":{"date-parts":[[2006,1,20]],"date-time":"2006-01-20T20:42:38Z","timestamp":1137789758000},"page":"1097-1105","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":13,"title":["Identification of Novel \u03b3\u03b4 T-Cell Subsets following Bacterial Infection in the Absence of V\u03b31\n                    <sup>+<\/sup>\n                    T Cells: Homeostatic Control of \u03b3\u03b4 T-Cell Responses to Pathogen Infection by V\u03b31\n                    <sup>+<\/sup>\n                    T Cells"],"prefix":"10.1128","volume":"74","author":[{"given":"Darren J.","family":"Newton","sequence":"first","affiliation":[{"name":"Research Institute of Molecular and Cellular Biology, University of Leeds, Leeds, United Kingdom"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Elizabeth M.","family":"Andrew","sequence":"additional","affiliation":[{"name":"Research Institute of Molecular and Cellular Biology, University of Leeds, Leeds, United Kingdom"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Jane E.","family":"Dalton","sequence":"additional","affiliation":[{"name":"Research Institute of Molecular and Cellular Biology, University of Leeds, Leeds, United Kingdom"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Rainy","family":"Mears","sequence":"additional","affiliation":[{"name":"Research Institute of Molecular and Cellular Biology, University of Leeds, Leeds, United Kingdom"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Simon R.","family":"Carding","sequence":"additional","affiliation":[{"name":"Research Institute of Molecular and Cellular Biology, University of Leeds, Leeds, United Kingdom"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"235","reference":[{"key":"e_1_3_1_2_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.micinf.2004.12.010"},{"key":"e_1_3_1_3_2","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.175.3.1741"},{"key":"e_1_3_1_4_2","doi-asserted-by":"publisher","DOI":"10.1016\/0092-8674(88)90139-0"},{"key":"e_1_3_1_5_2","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.174.8.4606"},{"key":"e_1_3_1_6_2","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.88.1.43"},{"key":"e_1_3_1_7_2","doi-asserted-by":"crossref","first-page":"4280","DOI":"10.4049\/jimmunol.156.11.4280","volume":"156","year":"1996","unstructured":"Belles, C., A. 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