{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,29]],"date-time":"2026-03-29T14:37:57Z","timestamp":1774795077310,"version":"3.50.1"},"reference-count":47,"publisher":"Wiley","issue":"2","license":[{"start":{"date-parts":[[2014,4,24]],"date-time":"2014-04-24T00:00:00Z","timestamp":1398297600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Immunology"],"published-print":{"date-parts":[[2014,6]]},"abstract":"<jats:title>Summary<\/jats:title><jats:p><jats:italic>Chlamydia trachomatis<\/jats:italic> urogenital serovars D\u2013K are intracellular bacterial pathogens that replicate almost exclusively in human reproductive tract epithelium. In the <jats:italic>C.\u00a0muridarum<\/jats:italic> mouse model for human <jats:italic>Chlamydia<\/jats:italic> genital tract infections <jats:styled-content style=\"fixed-case\">CD<\/jats:styled-content>4 T helper type 1 cell responses mediate protective immunity while <jats:styled-content style=\"fixed-case\">CD<\/jats:styled-content>8 T\u2010cell responses have been associated with scarring and infertility. Scarring mediated by <jats:styled-content style=\"fixed-case\">CD<\/jats:styled-content>8 T cells requires production of tumour necrosis factor\u2010<jats:italic>\u03b1<\/jats:italic> (<jats:styled-content style=\"fixed-case\">TNF<\/jats:styled-content>\u2010<jats:italic>\u03b1<\/jats:italic>); however, <jats:styled-content style=\"fixed-case\">TNF<\/jats:styled-content>\u2010<jats:italic>\u03b1<\/jats:italic> is associated with protective immunity mediated by <jats:styled-content style=\"fixed-case\">CD<\/jats:styled-content>4 T cells. The latter result suggests that <jats:styled-content style=\"fixed-case\">TNF<\/jats:styled-content>\u2010<jats:italic>\u03b1<\/jats:italic> in\u2010and\u2010of itself may not be the sole determining factor in immunopathology. <jats:styled-content style=\"fixed-case\">CD<\/jats:styled-content>8 T cells mediating immunopathology presumably do something in addition to producing <jats:styled-content style=\"fixed-case\">TNF<\/jats:styled-content>\u2010<jats:italic>\u03b1<\/jats:italic> that is detrimental during resolution of genital tract infections. To investigate the mechanism underlying <jats:styled-content style=\"fixed-case\">CD<\/jats:styled-content>8 immunopathology we attempted to isolate <jats:italic>Chlamydia<\/jats:italic>\u2010specific <jats:styled-content style=\"fixed-case\">CD<\/jats:styled-content>8 T\u2010cell clones from mice that self\u2010cleared genital tract infections. They could not be derived with antigen\u2010pulsed irradiated naive splenocytes; instead derivation required use of irradiated immune splenocyte antigen\u2010presenting cells. The <jats:italic>Chlamydia<\/jats:italic>\u2010specific <jats:styled-content style=\"fixed-case\">CD<\/jats:styled-content>8 T\u2010cell clones had relatively low cell surface <jats:styled-content style=\"fixed-case\">CD<\/jats:styled-content>8 levels and the majority were not restricted by <jats:styled-content style=\"fixed-case\">MHC<\/jats:styled-content> class Ia molecules. They did not express <jats:italic>Plac8<\/jats:italic>, and had varying abilities to terminate <jats:italic>Chlamydia<\/jats:italic> replication in epithelial cells. Two of the five <jats:styled-content style=\"fixed-case\">CD<\/jats:styled-content>8 clones produced interleukin\u201013 (<jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u201013) in addition to <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u20102, <jats:styled-content style=\"fixed-case\">TNF<\/jats:styled-content>\u2010<jats:italic>\u03b1<\/jats:italic>,<jats:styled-content style=\"fixed-case\"> IL<\/jats:styled-content>\u201010 and interferon\u2010<jats:italic>\u03b3<\/jats:italic>. <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u201013\u2010producing <jats:italic>Chlamydia<\/jats:italic>\u2010specific <jats:styled-content style=\"fixed-case\">CD<\/jats:styled-content>8 T cells may contribute to immunopathology during <jats:italic>C.\u00a0muridarum<\/jats:italic> genital tract infections based on known roles of <jats:styled-content style=\"fixed-case\">TNF<\/jats:styled-content>\u2010<jats:italic>\u03b1<\/jats:italic> and <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u201013 in scar formation.<\/jats:p>","DOI":"10.1111\/imm.12248","type":"journal-article","created":{"date-parts":[[2014,1,16]],"date-time":"2014-01-16T04:42:53Z","timestamp":1389847373000},"page":"248-257","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":39,"title":["An atypical <scp>CD<\/scp>8 T\u2010cell response to <i>Chlamydia muridarum<\/i> genital tract infections includes T cells that produce interleukin\u201013"],"prefix":"10.1111","volume":"142","author":[{"given":"Raymond M.","family":"Johnson","sequence":"first","affiliation":[{"name":"Department of Medicine Indiana University School of Medicine Indianapolis IN USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Micah S.","family":"Kerr","sequence":"additional","affiliation":[{"name":"Department of Medicine Indiana University School of Medicine Indianapolis IN USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"James E.","family":"Slaven","sequence":"additional","affiliation":[{"name":"Department of Biostatistics Indiana University School of Medicine Indianapolis IN USA"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"311","published-online":{"date-parts":[[2014,4,24]]},"reference":[{"key":"e_1_2_8_2_1","doi-asserted-by":"publisher","DOI":"10.1097\/OLQ.0b013e318286bb53"},{"key":"e_1_2_8_3_1","doi-asserted-by":"publisher","DOI":"10.1186\/1471-2334-13-388"},{"key":"e_1_2_8_4_1","unstructured":"Control. 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